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Novel Molecular Pathways in Oncology, 3rd Edition
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Novel Molecular Pathways in Oncology, 3rd Edition

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: 1 December 2025 | Viewed by 3183

Special Issue Editor

Dr. Giovanna Casili

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres, 31-98166 Messina, Italy
Interests: neuroinflammation; neurodegeneration; inflammation; oncology; brain tumor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oncology research continues to reveal the molecular signatures that define tumor characteristics and behavior, with the focus increasingly shifting toward the complex molecular pathways implicated in tumorigenesis, cancer cell proliferation, inflammation and angiogenesis, tissue infiltration, and dissemination to distant sites. New research should focus on better investigating the molecular mechanisms that promote cancer and on the development of efficient therapeutic and pharmacological interventions. For this Special Issue, we welcome research and review articles focusing on the diverse molecular mechanisms implicated in different steps of carcinogenesis, which could serve as therapeutic targets.

Dr. Giovanna Casili
Guest Editor

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Keywords

  • molecular pathway involved in tumorigenesis
  • cancer therapy
  • targeted therapy
  • anticancer drugs
  • brain cancer
  • oral cancer
  • gastrointestinal cancer

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Published Papers (3 papers)

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Research

13 pages, 3320 KiB  
Article
Regulation of Human Lung Adenocarcinoma Cell Proliferation by LncRNA AFAP-AS1 Through the miR-508/ZWINT Axis
by Sultan F. Kadasah and Abdulaziz M. S. Alqahtani
Int. J. Mol. Sci. 2025, 26(13), 6532; https://doi.org/10.3390/ijms26136532 - 7 Jul 2025
Viewed by 296
Abstract
Lung adenocarcinoma is a prevalent, aggressive cancer with a poor prognosis due to early metastasis and resistance to treatment. LncRNA AFAP1-AS1 has been shown to be associated with the development of multiple carcinomas. This study investigates the functional role of AFAP1-AS1 in lung [...] Read more.
Lung adenocarcinoma is a prevalent, aggressive cancer with a poor prognosis due to early metastasis and resistance to treatment. LncRNA AFAP1-AS1 has been shown to be associated with the development of multiple carcinomas. This study investigates the functional role of AFAP1-AS1 in lung adenocarcinoma cell proliferation via miR-508-3p and ZWINT. Human lung adenocarcinoma A549 cells were transfected with siRNA constructs against AFAP1-AS1 (si-AFAP1-AS1) to silence its expression. Cell proliferation was evaluated via CCK-8 and colony-forming assays. Apoptosis was assessed using AO/EB staining, and invasion was determined via Transwell assay. The interaction between AFAP1-AS1, miR-508-3p, and ZWINT was confirmed via dual luciferase reporter assay and qRT-PCR analysis. Data were analysed using appropriate statistical tests. AFAP1-AS1 was significantly upregulated in lung adenocarcinoma cells compared to normal BEAS-2B cells. Silencing of AFAP1-AS1 resulted in a marked reduction in A549 cell proliferation and colony development, as observed in CCK-8 and colony formation assays. The AO/EB assay showed a significant increase in apoptosis (30 ± 4.4%) in si-AFAP1-AS1 transfected cells compared to control si-NC (3 ± 1.2%). In addition, knockdown of AFAP1-AS1 led to an upsurge of pro-apoptotic Bax and decline of anti-apoptotic Bcl-2 expression. The dual luciferase assay established the interaction between AFAP1-AS1 and miR-508-3p. Furthermore, ZWINT, identified as a target of miR-508-3p, was significantly upregulated in lung adenocarcinoma tissues. Overexpression of ZWINT rescued the inhibitory effects of AFAP1-AS1 silencing on cell proliferation, colony formation, and apoptosis, while also reversing the reduction in cell invasion. AFAP1-AS1 accelerates the development of lung adenocarcinoma by cell proliferation, apoptosis, and invasion via the miR-508-3p/ZWINT axis. Thus, targeting AFAP1-AS1 or its downstream regulatory axis could offer novel therapeutic approaches in lung adenocarcinoma treatment. Full article
(This article belongs to the Special Issue Novel Molecular Pathways in Oncology, 3rd Edition)
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15 pages, 3764 KiB  
Article
Apoptosis-Inducing and Proliferation-Inhibiting Effects of Doramectin on Mz-ChA-1 Human Cholangiocarcinoma Cells
by Yunfang Zhang, Wei Wu, Yan Shi, Yuehong Huang, Ting Dai, Lina Ke, Lizhu Chen, Mingliang Chen and Qin Wang
Int. J. Mol. Sci. 2024, 25(24), 13440; https://doi.org/10.3390/ijms252413440 - 15 Dec 2024
Viewed by 1132
Abstract
Cholangiocarcinoma is a malignant tumor that emerges in the intrahepatic or extrahepatic bile ducts. Doramectin (DOR), a third-generation derivative of avermectins (AVMs), is renowned for its low toxicity and high efficiency. However, no research has hitherto focused on the anti-cholangiocarcinoma effects of these [...] Read more.
Cholangiocarcinoma is a malignant tumor that emerges in the intrahepatic or extrahepatic bile ducts. Doramectin (DOR), a third-generation derivative of avermectins (AVMs), is renowned for its low toxicity and high efficiency. However, no research has hitherto focused on the anti-cholangiocarcinoma effects of these drugs. In this study, we undertook a preliminary exploration of the mechanism through which DOR inhibits the viability of human cholangiocarcinoma cells (Mz-ChA-1) via transcriptome analysis and molecular validation at the cellular level. The results indicated that DOR could suppress the growth and proliferation of Mz-ChA-1 cells in a dose-dependent manner. Moreover, it significantly diminished their migration and invasion abilities. Cell cycle analysis disclosed arrest in the G1 phase, accompanied by an increase in p21 expression and a decrease in the levels of the cyclin E1 and CDK2 proteins. Additionally, DOR induced apoptosis via the ROS-triggered mitochondrial pathway. This was attested by an elevation in the BAX/BCL-2 ratio, the activation of caspase 3/7 and the cleavage of PARP1. These mechanistic insights underscore DOR’s potential as a therapeutic agent against cholangiocarcinoma Full article
(This article belongs to the Special Issue Novel Molecular Pathways in Oncology, 3rd Edition)
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16 pages, 6325 KiB  
Article
Echium amoenum and Rosmarinic Acid Suppress the Growth and Metastasis of Gastric Cancer AGS Cells by Promoting Apoptosis and Inhibiting EMT
by Mahdieh Ahmadi, Hong Lae Kim, So Jin Park and Hye Jin Jung
Int. J. Mol. Sci. 2024, 25(23), 12909; https://doi.org/10.3390/ijms252312909 - 30 Nov 2024
Cited by 1 | Viewed by 1415
Abstract
Gastric cancer (GC) ranks as the fifth most prevalent cancer globally. Owing to the absence of early manifest symptoms, it is difficult to diagnose GC until it has metastasized to other organs. Hence, the prevention and treatment of GC have become major concerns [...] Read more.
Gastric cancer (GC) ranks as the fifth most prevalent cancer globally. Owing to the absence of early manifest symptoms, it is difficult to diagnose GC until it has metastasized to other organs. Hence, the prevention and treatment of GC have become major concerns for patients. Echium amoenum, a traditional medicinal plant from the Boraginaceae family, exhibits various biological activities. Although recent studies have reported the anticancer properties of E. amoenum, its effects and mechanisms of action on GC cells are not yet fully understood. This study examined the anticancer effects of the ethyl acetate extract of E. amoenum (EAEC) and its main active ingredient, rosmarinic acid (RA), in GC AGS cells. EAEC and RA suppressed AGS cell growth by inducing apoptosis through caspase mediation and inhibited AGS cell metastasis by influencing the expression of crucial epithelial–mesenchymal transition (EMT) biomarkers. Furthermore, the anti-growth and anti-metastatic effects of EAEC and RA on AGS cells involved inactivation of the STAT3, AKT, and ERK1/2 pathways. Additionally, RA notably inhibited the in vivo tumor growth in AGS cells. Overall, these results indicate that EAEC and RA could serve as potential anticancer and anti-metastasis agents for GC. Full article
(This article belongs to the Special Issue Novel Molecular Pathways in Oncology, 3rd Edition)
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