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Advancing Cancer Research: Molecular Insights, Diagnostic Innovations and Therapeutic Targets
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Advancing Cancer Research: Molecular Insights, Diagnostic Innovations and Therapeutic Targets

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 2138

Special Issue Editor

Prof. Dr. Jue Wang

E-Mail Website
Guest Editor
Department of Internal Medicine, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd, Dallas, TX 75390, USA
Interests: molecular mechanisms; genitourinary cancer; cancer treatments; cancer prevention; reduce treatment-related toxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a call for submissions for a Special Issue focused on new molecular insights into carcinogenesis, molecular pathology, and their translational potential in cancer diagnosis, imaging, and treatment. This issue aims to showcase cutting-edge research that bridges the gap between molecular science and clinical applications, paving the way for novel diagnostic tools, therapeutic targets, and precision oncology.

We invite original research articles, reviews, and perspectives in the following areas:

  • Molecular Insights into Carcinogenesis:
    • Genetic and epigenetic drivers of cancer initiation and progression;
    • Insights into tumor heterogeneity and clonal evolution;
    • Mechanistic studies of cancer-related pathways.
  • Innovations in Molecular Pathology:
    • Integration of molecular findings into histopathology;
    • Role of liquid biopsy in molecular pathology.
  • Novel Cancer Diagnostics and Imaging:
    • Molecular imaging modalities and their clinical implications;
    • Development of biomarkers for early detection;
    • AI-driven approaches in cancer imaging and pattern recognition.
  • Novel Therapeutic Targets and Biomarkers:
    • Discovery and validation of predictive and prognostic biomarkers;
    • Development of cancer-agnostic biomarkers;
    • Therapeutic implications of targetable mutations and pathways.
  • Applications of Artificial Intelligence (AI):
    • AI in drug discovery and biomarker development;
    • Machine learning models for prognosis and treatment prediction;
    • Integration of AI into clinical decision-making.

We look forward to receiving your contributions.

Prof. Dr. Jue Wang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer
  • carcinogenesis
  • molecular pathology
  • signaling transduction
  • diagnosis
  • treatment
  • prognosis
  • pathogenesis
  • precision oncology
  • biomarker discovery
  • genomic profiling

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Published Papers (2 papers)

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Research

19 pages, 3769 KiB  
Article
Metabolic Reprogramming of Urothelial Carcinoma—A Theragnostic Target for Betulinic Acid
by Anirban Ganguly, Aratrika Halder, Keara Healy, Stephanie Daugherty, Shingo Kimura, Rajkumar Banerjee, Jonathan M. Beckel and Pradeep Tyagi
Int. J. Mol. Sci. 2025, 26(12), 5598; https://doi.org/10.3390/ijms26125598 - 11 Jun 2025
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Abstract
A pivotal role of metabolic reprogramming in urothelial carcinoma is hallmarked by the dependence of two-fold faster proliferation of urothelial carcinoma cell line T24 than benign cell line TRT-HU1 on five-fold higher glucose (basal) 16 mM vs. 3 mM in McCoy’s 5A media [...] Read more.
A pivotal role of metabolic reprogramming in urothelial carcinoma is hallmarked by the dependence of two-fold faster proliferation of urothelial carcinoma cell line T24 than benign cell line TRT-HU1 on five-fold higher glucose (basal) 16 mM vs. 3 mM in McCoy’s 5A media and Keratinocyte Serum Free media, respectively. Here, we report that an additional 10% increase to 17.6 mM and 3.3 mM glucose significantly shortens the doubling time by 3 h and 1 h for T24 and TRT-HUI, respectively. T24 grown at 17.6 mM glucose lowers the confocal localization of the fatty acid mimetic, Betulinic Acid (BA) conjugated to FITC (BA-FITC) with Mito Tracker Red (mitochondrial marker), which doubles the IC50 of BA and BA-FITC by lowering cell cycle arrest in the G0/G1 phase from 54.2% to 43.8% and caspase-3/7 mediated apoptosis and by reversing caspase-3, p53, PTEN, GAPDH, and XIAP gene expression induced by BA in T24 grown at basal glucose (16 mM). Besides slowing the glycogen and pH decline of T24 at basal glucose, BA exhibited an eight-fold higher IC50 than Mitomycin C (MC) on TRT-HU1 by not mimicking the glucose-insensitive cycle arrest and apoptosis of MC. Overall, the glucose sensitivity of the lower IC50 of BA-FITC and BA on T24 vs. TRT-HU1 supports the safety of BA conjugates for theragnostic purposes. Full article
(This article belongs to the Special Issue Advancing Cancer Research: Molecular Insights, Diagnostic Innovations and Therapeutic Targets)
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13 pages, 7512 KiB  
Article
High Mobility Group Box 1 Is Potential Target Therapy for Inhibiting Metastasis and Enhancing Drug Sensitivity of Hepatocellular Carcinoma
by Arunya Jiraviriyakul, Chatchai Nensat, Samitanan Promchai, Yanisa Chaiaun, Yanisa Hoiraya, Nutnicha Yamnak, Suphakit Khutanthong, Nun Singpan and Worawat Songjang
Int. J. Mol. Sci. 2025, 26(8), 3491; https://doi.org/10.3390/ijms26083491 - 8 Apr 2025
Viewed by 1307
Abstract
Hepatocellular carcinoma (HCC) is a lethal malignancy associated with drug resistance, resulting in a poor prognosis. High mobility group box 1 (HMGB1) is a chromatin-binding protein that regulates HCC progression. The overexpression of HMGB1 has been found to promote tumorigenesis and drug resistance. [...] Read more.
Hepatocellular carcinoma (HCC) is a lethal malignancy associated with drug resistance, resulting in a poor prognosis. High mobility group box 1 (HMGB1) is a chromatin-binding protein that regulates HCC progression. The overexpression of HMGB1 has been found to promote tumorigenesis and drug resistance. In this study, we aimed to investigate the role of HMGB1 expression in tumorigenesis and metastasis and its impact on sorafenib and oxaliplatin resistance. Tissue samples from patients with HCC (n = 48) were subjected to immunohistochemistry. The expression of HMGB1 was correlated with clinical pathology parameters. Moreover, the HCC cell line HuH-7 was used to study the regulatory effect of HMGB1 on cell proliferation, cell adhesion, migration, and invasion by using the siRNA (small interfering RNA) silencing method. Furthermore, drug challenges were performed to determine the effect of HMGB1 on the sensitivity to chemotherapeutic drugs (sorafenib and oxaliplatin). HMGB1 was significantly overexpressed in tumor tissues, highlighted by the expression increment in patients with M1 advanced metastasis tumors with immunoreactivity scores 2.61 and 6.50 for adjacent and tumor tissues, respectively (p-values = 0.0035). The involved mechanisms were then described through the suppression of HCC cell adhesion, migration, and invasion by HMGB1 silencing. Notably, the inhibition of HMGB1 expression promoted sorafenib/oxaliplatin sensitivity in the HCC cell line by increasing the cell toxicity by about 13–18%. Our study demonstrated that HMGB1 shows potential as a promising biomarker and a target for HCC treatment that is involved in tumorigenesis, metastasis, and chemo-drug resistance. Full article
(This article belongs to the Special Issue Advancing Cancer Research: Molecular Insights, Diagnostic Innovations and Therapeutic Targets)
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