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Article

Exploring the Oncogenic Potential of Bisphenol F in Ovarian Cancer Development

by
Hussein Sakr
1,
Amira Al Kharusi
1,
Shika Hanif Malgundkar
2 and
Srinivasa Rao Sirasanagandla
3,*
1
Physiology Department, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman
2
Biochemistry Department, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman
3
Human and Clinical Anatomy Department, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman
*
Author to whom correspondence should be addressed.
Appl. Sci. 2025, 15(10), 5561; https://doi.org/10.3390/app15105561
Submission received: 12 April 2025 / Revised: 5 May 2025 / Accepted: 10 May 2025 / Published: 15 May 2025
(This article belongs to the Special Issue Exposure Pathways and Health Implications of Environmental Chemicals)
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Abstract

Ovarian cancer (OC) is a gynecological cancer characterized by high morbidity and mortality associated with poor survival outcomes. Bisphenol F (BPF), a widely used analog of bisphenol A (BPA), has recently gained attention due to its potential endocrine-disrupting properties and ubiquitous environmental presence. However, the carcinogenic potential of BPF in OC has not been well explored. This study investigates the effects of BPF on ovarian carcinogenesis by assessing its pathological impact on cellular processes, including cell proliferation, wound healing, and cell invasion. OC cells, SKOV3 were treated with varying concentrations of BPF (0.01–250 µM). Cell viability was assessed using Alamar Blue assay, and migration ability was analyzed using wound-healing assay. Further, the total antioxidative capability (T-AOC) was measured. Statistical analysis was performed using student’s-t-test/ANOVA, with a significance set at p < 0.05. BPF exhibited a dual role in cell viability, enhancing cell proliferation at low concentrations (1 µM: p = 0.034; 10 µM: p = 0.012) while exerting cytotoxic effects at higher concentrations (250 µM: p = 0.021). Further, a wound-healing assay demonstrated that a lower concentration, 1 µM BPF promoted cell migration (p = 0.0345), indicating its involvement in OC. However, a non-significant difference was observed in the invasive potential and T-AOC of BPF-treated SKOV3 cells. Our findings provide key insights into the effects of BPF on cellular processes linked with ovarian carcinogenesis, emphasizing the need for future experiments to comprehend its mechanisms of action.

1. Introduction

Globally, ovarian cancer (OC) is the eighth most common cancer with 324,603 incident cases and 206,956 deaths [1]. The five-year survival rate for early-stage OC patients is 93%, as opposed to only 31% for those diagnosed at advanced stages, emphasizing the importance of early detection [2] for improving survival outcomes. In the past few years, bisphenol-A (BPA), a commonly used chemical for polycarbonate plastic production dating back to the 1950s, has been linked with cytotoxicity [3,4], thereby regarding it as a public health concern.
Human exposure to bisphenol is primarily attributed to its gradual degradation into its monomeric form [5], prompting several regulatory bodies to impose restrictions on its use [5]. This has led to increased use of BPA analogs, including BPS, Bisphenol F (BPF), and BPAF. Although initially discovered as a safer alternative to BPA, the eight BPA analogs, including BPF have been implicated in potentially adverse health effects [6,7,8].
There has been a surge in epidemiological studies exploring the association between bisphenol exposure and cancer risk. Higher urinary levels of BPA and BPS were significantly associated with an increased risk of developing lung cancer, particularly in men [9]. Similarly, elevated urinary BPA levels were associated with a higher risk of prostate cancer [10], and non-small cell lung cancer [11].
BPA contributes to tumor development by modulating cellular properties such as cell proliferation, migration and cell death by regulating various cancer signaling cascades such as PI3K/AKT, MAPK, and STAT3 pathways [12]. In papillary thyroid cancer, BPA reduced E-cadherin levels and increased vimentin levels, thereby inducing epithelial-mesenchymal transition, and cell invasiveness [13]. In OC, BPA-enhanced cell proliferation, invasion and migration through Erα/AKT/mTOR, HIF-1α cascade [14]. Similar to BPA, BPS regulates key cellular features involved in carcinogenesis. BPS promoted cell proliferation and induced elevated levels of vascular endothelial growth factor as well as stem cell marker (CD44) in breast cancer [15]. Further, BPS enhanced cell proliferation and invasion in prostate cancer [16], and migration in non-small cell lung cancer [17]. In OC, BPS and BPA promoted cancer cell stemness through the PINK1/p53 mitophagic cascade [18].
BPF is widely used in the manufacturing of epoxy resins, constituted in materials such as water pipes, plastics, varnishes and food containers [19]. Owing to its structural resemblance to BPA, BPF has been regarded as an endocrine-disrupting chemical [19]. Further, given the widespread occurrence in the environment, BPF has been detected in human biological samples, posing a threat to human health [20]. In a previous study, over 85% of urine samples from healthy individuals tested positive for BPF [5]. Similarly, another finding demonstrated the presence of urinary BPF in 42–88% of U.S. adults [21].
A wide range of health conditions such as cardiovascular diseases [22,23], autoimmune disorders [24], diabetes, neurodegenerative issues [25,26], metabolic disorders [27] and cancer [28,29], have been reported to have an association with BPF [19,30]. Zhou et al. (2023) [31] observed enhanced cell apoptosis and reduced cell survival in BPF-treated mouse TM3 Leydig cells, indicating the detrimental effects of BPF on the reproductive system. Further, BPF promoted intracellular ROS formation and reduced Nrf2 levels [31]. Surprisingly, intrinsic and extrinsic apoptosis was activated by BPF in human placental cells, thereby inducing cytotoxicity [32]. Similarly, BPF promoted apoptosis in osteoblasts, thereby preventing cell proliferation and affecting bone health [33].
The widespread detection of BPF in human urine and its function as an endocrine disruptor has raised concerns regarding potential involvement in tumorigenesis. Elevated BPF levels have been documented in papillary thyroid cancer [34]. Additionally, BPF enhanced ovarian granulosa tumor cell proliferation, invasion, and glucose uptake [35]. In breast cancer cell line MCF-7, a dual role of BPF was observed, with a dose of 0.01–1 µM promoting cell viability and a high dose (25 and 50 µM) exerting cytotoxic effect [36]. Owing to the increasing environmental exposure to BPF and their potential function in tumorigenesis, evaluating the cytotoxic effects of BPF in OC is pivotal.
Despite the rising prevalence of BPF in the environment and its increasing use as a BPA alternative, very few studies have elucidated the adverse effects of BPF in OC [37]. Hence, investigating the effects of BPF on ovarian carcinogenesis is essential to understanding its mechanism of action and the need for its restricted use in the plastic industries. The present study aims to elucidate the potential involvement of BPF in ovarian carcinogenesis by assessing its impact on key cellular processes such as cell proliferation, migration, and invasion assays. These functional approaches provide a comprehensive understanding of BPF’s impact on OC, thereby highlighting its role as a potential environmental risk factor.

2. Materials and Methods

2.1. Cell Culture and BPF Treatment

OC cell line, SKOV3, was cultured in Roswell Park Memorial Institute (RPMI) 1640 growth media (Gibco, Grand Island, NY, USA) in the presence of 10% FBS (Gibco, Grand Island, NY, USA), and 1% penicillin/streptomycin antibiotic in an incubator maintained at 37 °C and 5% CO2. BPF was purchased from Sigma Aldrich (Catalog number: 51453-100 mg, Saint Louis, MO, USA), and dissolved in 1 mL dimethyl sulfoxide (DMSO) (Sigma, Saint Louis, MO, USA) to prepare a stock solution of 499.5 mM. A range of BPF dilutions (0.01–250 µM) were prepared in DMSO. Moreover, 100 µM of working solution of BPF was prepared in DMSO, and 0.1, and 1 µL of this solution was added to a total of 100 µL plain media to achieve 0.1 and 1 µM final BPF concentrations, respectively. To obtain a final concentration of 10–100 µM BPF in a total of 100 µL plain media, 10 mM working solution of BPF was prepared and 0.1, 0.2, 0.3–1.0 µL of the working solution was added. Meanwhile, 50 mM working solution was prepared to reach 150 and 250 µM BPF concentrations by diluting 0.3 and 0.5 µL, respectively, in a total of 100 µL plain media. For negative control (NC), the cells were treated with the same volume of DMSO only.

2.2. Alamar Blue Assay

SKOV3 cells were seeded in a 96-well plate (Thermo Fisher Scientific, Roskilde, Denmark) at a density of 5.5 × 103 per well and propagated for 24 h. Then, the cells were treated with a range of BPF concentrations (0.01–250 µM) for 24 h to investigate its effects on ovarian carcinogenesis. Cells treated with an equal volume of DMSO only were used as the NC. The following day, the media was replaced with 100 µL fresh media, and 10 µL Alamar blue dye (Thermofisher Scientific, Eugene, OR, USA) was added and incubated for 3 h. The absorbance was subsequently measured at 570 nm wavelength (600 nm reference) using a BioTek Synergy H1 multiplate reader (BioTek Instruments Inc., Winooski, VT, USA). Cell viability was calculated as follows [38]:
C e l l   v i a b i l i t y   % = mean   OD   of treated   cell   − mean   OD   of   blank mean   OD   of   untreated   cell NC − mean   OD   of   blan × 100

2.3. In Vitro Wound-Healing Assay

To assess the migratory capacity of OC cells SKOV3, an in vitro wound-healing assay was performed following BPF treatment. SKOV3 cells were plated in 24-well plates at a density of 4 × 104 cells per well and allowed to reach approximately 70% confluency the next day. The cells were then treated with 1 µM BPF/10 µM BPF/NC (DMSO). A scratch was introduced into the cell monolayer using a sterile 10 µL pipette tip. The cells were rinsed with PBS to remove the detached cells, and a fresh medium was added. Images of the wound area were captured at 0, 24, and 48 h post-incubation using a Zeiss Axiovert 25 (Carl Zeiss Microscopy GmbH, Jena, Germany) at 10× magnification [39]. The width of the wound gap was measured using ImageJ software (Version 1.53t) at different time points following wound induction in SKOV3 cells by drawing a straight line across the cell-free wound region using the line tool. Three measurements were taken per image, and the extent of wound closure was measured using the formula:
[Wo − Wt]/Wo × 100
  • Wo = Initial wound width at 0 h
  • Wt = Wound width at later time point (24 or 48 h)

2.4. Cell Invasion Assay

The effect of BPF treatment on invasive potential of SKOV3 cells was assessed using cell invasion assay kit (Catalog: ECM551, Merck, Saint Louis, MO, USA). Briefly, SKOV3 cells were seeded in a 6-well plate at a cell density of 1.5 × 105 such that it reached 70% confluency after 24 h. The following day, the cells were treated with 1 µM BPF/10 µM BPF/DMSO (NC) in serum-free RPMI media for 24 h, washed twice with PBS, trypsinized using 500 µL of 0.05% trypsin-EDTA harvesting buffer, resuspended in 2 mL quenching media containing BSA, MgCl2, and CaCl2 and seeded into the upper chamber of the trans-well insert at a density of 2 × 104 cells (prepared in FBS free media). Moreover, 500 µL of serum-containing RPMI media was added to the lower chamber, and the cells were incubated for 24 h. Following incubation, the cell suspension was removed from the interior of the inserts, and the inserts were placed in 400 µL cell stain for 20 min at room temperature. After washing the inserts, they were cleaned with swabs to remove non-invading cells, air-dried, and placed in 200 µL of extraction buffer for 15 min at room temperature. Moreover, 100 µL of the dye mixture was pipetted into a 96-well plate, and the absorbance was measured at 560 nm using a BioTek Synergy H1 multiplate reader. The absorbance reflected the number of invaded cells [40].

2.5. Total Anti-Oxidative Capability Assay

The T-AOC assay was performed according to the manufacturer’s guidelines (Catalog number: SH0148). Briefly, SKOV3 cells were cultured in T75 flasks for 24 h, and treated with 1 µM BPF/DMSO (NC) in plain RPMI media for 24 h. Subsequently, after discarding the media, the cells were washed twice with cold PBS, and protein was extracted using RIPA lysis buffer (Thermofisher Scientific, Rockford, IL, USA) along with protease/phosphatase inhibitor. The plate was placed on ice, the cells were scraped after adding the lysis buffer, the lysate was vortexed every 1–2 min for 30 min, and centrifuged at 14,000× g for 15 min at 4 °C. Protein concentrations (supernatant) were measured using BCA (Thermofisher Scientific, Rockford, IL, USA).
Then, the sample tube was prepared by combining 1 mL of Reagent 1, 200 µL of homogenate, 2 mL of R2 and 500 µL of R3 working solutions. The mixture was subjected to vortex and incubated at 37 °C in a water bath for 30 min. Next, 200 µL of both R4, and R5 reagents were added, and the tube was incubated for 10 min at room temperature. Similarly, the contrast tube was prepared by combining 1 mL of Reagent1, 2 mL of R2 and 500 µL of R3 working solutions, placed in water bath at 37 °C, mixed with 200 µL each of R4, R5 reagents and homogenate and incubated at room temperature for 10 min. The OD was then measured at 520 nm.

2.6. Statistical Analysis

Data are represented as mean ± SD. The normality of the data were tested using the Shapiro–Wilk test; subsequently, the differences in the two groups were analyzed using Student’s t-test (normally distributed data) and/or Mann–Whitney test for non-parametric data. The ANOVA (normally distributed data) followed by the Dunnett test was used for more than two groups. The statistical significance was set at p < 0.05. All cell culture experiments were performed in triplicates in at least three independent experiments.

3. Results

3.1. Dose-Dependent Effects of BPF on Ovarian Cell Viability

To explore the impact of BPF on ovarian carcinogenesis, a 24-h cell viability assay was performed using a range of BPF concentrations (0.01–250 µM). The results suggest a concentration-dependent effect of BPF on cell viability (Figure 1). Low BPF concentrations (1 µM; p = 0.034 and 10 µM; p = 0.012) enhanced cell viability slightly by approximately 10.4% and 7.6%, respectively, compared to the control, while higher concentrations (250 µM; p = 0.021) reduced cell viability by 39.2%, demonstrating cytotoxic effects.

3.2. BPF-Induced Concentration-Dependent Morphological Changes in SKOV3 Cells

The microscopic view of SKOV3 cells treated with varying concentrations of BPF compared to NC revealed that low BPF concentrations (1 µM and 10 µM) had minimal effect on cell morphology. While higher BPF concentration (250 µM) resulted in cytotoxic effects including cell rounding and detachment (Figure 2).

3.3. BPF Enhances Cell Migration Without Altering Invasive Behavior of OC Cells

Metastasis is a complex process that involves cell migration and invasion, key characteristics of cancer [41]. To determine the effect of BPF on cell migration, a wound-healing assay was performed. Cells treated with 1 µM BPF exhibited a 13.5% increase in migratory ability (p = 0.0345) compared to untreated cells, as demonstrated by enhanced wound closure (Figure 3).
The invasiveness of OC cells following BPF treatment was evaluated to determine its effect on metastatic behavior. Moreover, 1 µM and 10 µM BPF treatment did not alter the invasive ability compared to the NC (p = 0.344) (Figure 4).

3.4. BPF Does Not Alter T-AOC in OC Cells

One of the key mechanisms in cytotoxicity is oxidative stress, and antioxidant capacity is important to protect the cells from oxidative damage. Previously, BPF has been implicated in generating reactive oxygen species (ROS) [42,43]. Therefore, to identify the impact of BPF treatment on oxidative balance, T-AOC was analyzed. The assay revealed no significant difference in T-AOC in 1 µM BPF-treated cells compared to NC (p = 0.8087) (Figure 5).

4. Discussion

In the past few years, BPA has been increasingly substituted by BPF in consumer products due to safety issues. However, numerous investigations suggest the oncogenic potential of BPF, necessitating its comprehensive analysis in cancer development. This study aimed to evaluate BPF’s contribution to ovarian carcinogenesis, revealing its concentration-dependent effects on cell behavior. The findings demonstrated that BPF slightly enhanced cell viability at low concentrations, while at high concentrations, BPF imparted cytotoxic effects, indicating its ability to induce cell death.
The enhanced SKOV3 cell viability observed at low BPF concentrations aligns with previous findings in breast cancer [36]. For instance, BPF at 0.01–1 µM concentrations enhanced breast cancer cell proliferation. Furthermore, BPF increased the intracellular ROS and Ca2+ levels in MCF7 breast cancer cells. Moreover, increased protein expression levels of nuclear estrogen receptor (Erα), membrane estrogen receptor GPER1, cell cycle markers (cyclin D1 and c-myc), phosphor-ERK1/2, and PKB were observed at these BPF concentrations [44]. Similar molecular alterations might contribute to the enhanced cell viability observed in our findings at low BPF concentrations.
Contrary to our findings, Bujnakova Mlynarcikova & Scsukova, (2024) [37] reported that BPF had no significant effect on cell viability in CaOV3 ovarian cancer cells (IC50 > 200 µM). However, consistent with our observations, at higher concentrations (25 µM and 50 µM) BPF inhibited cell viability [36]. The variations in the effects of BPF in various OC cell lines could be attributed to the differences in their molecular profiles [45]. SKOV3 cells are characterized by mutations in PIK3CA, ARID1A and amplification in ERBB2 genes, while only TP53 is mutated in the CaOV3 cell line [45], which could contribute to observed cell line-specific effects.
Using bioinformatics approaches, Huang et al. (2024) [46] identified 276 potential targets including BCL2, CASP3, and MAPK3 linked with BPF-induced cellular alterations in prostate models. Further, functional enrichment analysis revealed these targets’ involvement in endocrine signaling, apoptosis, and cancer-related signaling cascades. Thereby, suggesting that BPF might promote prostate carcinogenesis by affecting cell death, proliferation, and androgen metabolism [46]. Our observations of enhanced proliferation and migration in OC cells at low BPF concentrations could be linked to the alterations of the BPF targets, by modulating the MAPK signaling cascade, inhibiting apoptosis, and promoting OC.
Cancer metastasis, a crucial hallmark of cancer [47], is a multistep process characterized by cell migration and invasion [41], accounting for a majority of cancer-related mortalities [48]. Recent reports suggest that environmental chemicals such as BPA [49] and BPF modulate cancer cell migration [28]. Therefore, we conducted a wound-healing assay to investigate its potential role in regulating metastatic cell behavior in OC. The assay results showed 13.5% enhanced cellular migration in the presence of 1 µM BPF, suggesting its potential role in facilitating OC progression. This aligns with previous findings in breast cancer, with enhanced cell migration in BPF-treated cells by modulating epithelial-mesenchymal transition markers and cell cycle-related genes [28]. Hence, the concentration-dependent effects observed in our study highlight the importance of understanding environmental exposure to BPF and its impact on ovarian tumorigenesis.
Invasion is a critical step in cancer metastasis, facilitating the cancer cells to migrate to distant organs, thereby promoting cancer progression [50]. Previously, BPA, a structural analog of BPF, was reported to enhance OC invasion. To determine whether BPF imparts similar effects in OC, an invasion assay was performed. The analysis revealed a non-significant difference in the SKOV3 cell invasiveness post-BPF treatment indicating the presence of alternative mechanisms of BPF-induced carcinogenesis. The observation of enhanced migration and non-invasiveness could be attributed to the differential modulation of the signaling cascades governing ECM degradation/MMP activation and cytoskeletal destabilization/motility.
Oxidative stress is the disruption in the balance between the antioxidant system and ROS [51]. Elevated levels of ROS, primary oxidants promoting oxidative stress, are key contributors to cancer and are known to enhance cancer cell proliferation and metastasis [52,53]. Due to the structural similarity between BPA and BPF, their biological effects could be analogous, including oxidative stress generation. Deng et al. (2021) demonstrated a positive association between BPA and oxidative stress markers as well as colorectal cancer risk [54]. In ovarian cells, BPA-enhanced ROS levels resulting in reduced antioxidant responses [55]. Further, in breast cancer, BPF treatment enhanced ROS and intracellular calcium levels [36].
To further understand the potential mechanisms of BPF-induced effects, we monitored T-AOC as a measure of oxidative stress response. While previous studies suggest that BPF generates ROS, our findings revealed no significant changes at 1 µM concentration, indicating that oxidative stress might not be the primary mechanism of BPF-induced cellular effects.
Moreover, these results underscore the need for further investigation into the molecular mechanisms underlying BPF’s actions. Future research should focus on elucidating the molecular mechanisms and signaling cascades through which BPF regulates proliferation and migration, such as the PI3K/AKT, MAPK/ERK, and estrogen-receptor-mediated pathways underlying BPF’s effects in OC. For identifying novel targets post-BPF exposure, transcriptomic and proteomic are crucial. Moreover, future studies to assess its long-term effects in vivo are required to have physiologically relevant insights. Such efforts will be crucial in determining whether BPF exposure poses a significant risk in cancer development. These findings would contribute to the development of safer, non-toxic BPF alternatives. Also, understanding environmental risk factors such as BPF enhances prevention strategies, and allows early-stage detection.
The limitation of the study is the use of only the SKOV3 cell line, which may not represent the OC heterogeneity. In addition, in vivo validation of the oncogenic potential of BPF in OC would further increase the impact of the study.

5. Conclusions

The significance of this study lies in addressing an urgent public health concern: the increasing incidence and mortality rates of OC. With the shift from BPA to BPF in commercial products due to safety issues, there is a need to evaluate the potential risks posed by BPF exposure. Despite its widespread use, BPF’s function as an endocrine disruptor and its involvement in cancer remain poorly understood. This research provides evidence that BPF can alter key cellular processes involved in ovarian carcinogenesis, including proliferation and migration. The observed effects on cell viability with enhanced growth at low concentrations reflect BPF’s contribution to ovarian tumorigenesis at environmentally relevant concentrations. Additionally, the finding that BPF promotes cell migration emphasizes its possible role in cancer progression and metastasis. Hence, this research lays the foundation for a better understanding of the environmental factors contributing to OC, intending to improve prevention, diagnosis, and treatment strategies.
Moreover, these results underscore the need for further investigation into the molecular mechanisms underlying BPF’s actions. Future research should focus on elucidating the pathways affected by BPF, and assessing its long-term effects in vivo. Such efforts will be crucial in determining whether BPF exposure poses a significant risk in cancer development.

Author Contributions

Conceptualization, H.S. and S.R.S.; methodology, H.S., S.H.M. and S.R.S.; validation, H.S., A.A.K. and S.R.S.; formal analysis, S.H.M.; data curation, S.H.M.; writing—original draft preparation, S.H.M.; writing—review and editing, S.R.S., H.S. and A.A.K. All authors have read and agreed to the published version of the manuscript.

Funding

The research was funded by the Sultan Qaboos University Deanship of Research (RF/MED/PHY/01/24).

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

The datasets analyzed or generated during the study are included in the manuscript.

Acknowledgments

The cells were kindly given by Aikou Okamoto from The Jikei University School of Medicine, Japan. For language enhancement, ChatGPT, GPT-4-Turbo model (2025) was used.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
BPABisphenol A
BPFBisphenol F
DMSODimethyl Sulfoxide
NCNegative Control
OCOvarian cancer
ROSReactive Oxygen Species

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Figure 1. Effects of varying concentrations of BPF on SKOV3 cell viability. A slight increase in cell viability was observed at lower BPF concentrations (1 µM and 10 µM), while at higher concentrations a reduction in cell viability was evident. Data represent mean ± SD from at least 3 experiments. * p < 0.05 compared to NC.
Figure 1. Effects of varying concentrations of BPF on SKOV3 cell viability. A slight increase in cell viability was observed at lower BPF concentrations (1 µM and 10 µM), while at higher concentrations a reduction in cell viability was evident. Data represent mean ± SD from at least 3 experiments. * p < 0.05 compared to NC.
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Figure 2. Microscopic images of SKOV3 cells treated with (A) DMSO (NC) and (B) 1 µM, (C) 10 µM and (D) 250 µM BPF concentrations. Low BPF concentrations (1 µM, 10 µM) had minimal effects on the cell morphology, while high concentration induced cell rounding compared to the control (Magnification 10×; Scale bar 1000 µm).
Figure 2. Microscopic images of SKOV3 cells treated with (A) DMSO (NC) and (B) 1 µM, (C) 10 µM and (D) 250 µM BPF concentrations. Low BPF concentrations (1 µM, 10 µM) had minimal effects on the cell morphology, while high concentration induced cell rounding compared to the control (Magnification 10×; Scale bar 1000 µm).
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Figure 3. Effect of BPF on cell migration. (A) Representative microscopic images of the wound area at 0 and 72 h for negative control (NC) and cells treated with 1 µM BPF. Magnification 10×, Scale bar = 1000 µm. (B) Quantification of the percentage of gap closure at 72 h. Cells treated with 1 µM BPF showed significantly higher wound closure compared to NC (p = 0.0345). Data are presented as mean ± SD (n = 3). * p < 0.05 compared to NC.
Figure 3. Effect of BPF on cell migration. (A) Representative microscopic images of the wound area at 0 and 72 h for negative control (NC) and cells treated with 1 µM BPF. Magnification 10×, Scale bar = 1000 µm. (B) Quantification of the percentage of gap closure at 72 h. Cells treated with 1 µM BPF showed significantly higher wound closure compared to NC (p = 0.0345). Data are presented as mean ± SD (n = 3). * p < 0.05 compared to NC.
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Figure 4. Effect of BPF on cell invasion. Cells treated with 1 µM and 10 µM BPF had no significant difference in cell invasive ability in comparison to NC (p = 0.344). Data are presented as mean ± SD (n = 3).
Figure 4. Effect of BPF on cell invasion. Cells treated with 1 µM and 10 µM BPF had no significant difference in cell invasive ability in comparison to NC (p = 0.344). Data are presented as mean ± SD (n = 3).
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Figure 5. T-AOC in cells treated with BPF. No significant difference in T-AOC was observed between BPF-treated cells and NC (p = 0.8087). Data are presented as mean ± SD (n = 3).
Figure 5. T-AOC in cells treated with BPF. No significant difference in T-AOC was observed between BPF-treated cells and NC (p = 0.8087). Data are presented as mean ± SD (n = 3).
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Sakr, H.; Al Kharusi, A.; Malgundkar, S.H.; Sirasanagandla, S.R. Exploring the Oncogenic Potential of Bisphenol F in Ovarian Cancer Development. Appl. Sci. 2025, 15, 5561. https://doi.org/10.3390/app15105561

AMA Style

Sakr H, Al Kharusi A, Malgundkar SH, Sirasanagandla SR. Exploring the Oncogenic Potential of Bisphenol F in Ovarian Cancer Development. Applied Sciences. 2025; 15(10):5561. https://doi.org/10.3390/app15105561

Chicago/Turabian Style

Sakr, Hussein, Amira Al Kharusi, Shika Hanif Malgundkar, and Srinivasa Rao Sirasanagandla. 2025. "Exploring the Oncogenic Potential of Bisphenol F in Ovarian Cancer Development" Applied Sciences 15, no. 10: 5561. https://doi.org/10.3390/app15105561

APA Style

Sakr, H., Al Kharusi, A., Malgundkar, S. H., & Sirasanagandla, S. R. (2025). Exploring the Oncogenic Potential of Bisphenol F in Ovarian Cancer Development. Applied Sciences, 15(10), 5561. https://doi.org/10.3390/app15105561

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