Molecular and Genetic Mechanism of Tumorigenesis

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (1 April 2022) | Viewed by 4114

Special Issue Editors


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Guest Editor
School of Life Science and Technology, Tongji University, Shanghai, China
Interests: cell proliferation; migration; apoptosis; tumorigenesis; tumor invasion

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Co-Guest Editor
School of Medicine, Nantong University, Nantong, Jiangsu, China
Interests: DNA damage response; cell cycle; apoptosis

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Co-Guest Editor
School of Life Science, Nankai University, Tianjin, China
Interests: The Hippo pathway; signal transduction; organ size control; tumorigenesis

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Co-Guest Editor
School of Medicine, Tongji University, Shanghai, China
Interests: tumorigenesis; metastasis; miRNA; cell death; cancer therapy

Special Issue Information

Dear Colleagues,

Cancer is one of the most fatal diseases that threaten human health, whereas more than 90% mortality of cancer patients is caused by tumor metastasis, rather than the growth of primary tumors. Understanding the molecular mechanism of tumor growth and progression is of great significance for cancer therapy.

Tumorigenesis is the gain of malignant properties in normal cells. Somatic copy-number changes, variants and mutations in genomic regions, and epigenetic modifications, etc., have been associated with tumorigenesis. Tumor metastasis is a process of cancer cells disseminating from a primary lesion via lymphatic and/or blood circulations to distal organs, which involves a variety of cellular mechanisms. Over the past decades, great progress has been made in exploring the mechanisms of tumor progression, in which numerous oncogenes, tumor suppressor genes, and multiple signaling pathways (e.g., Raf-MAPK, JNK, WNT, Hippo, Notch, JAK-STAT, and PI3K/AKT) have been implicated in tumor growth and metastasis. However, many questions still remain unanswered about the precise mechanism underlying tumorigenesis and metastasis.

In this Special Issue, we welcome original research, reviews, perspective and opinion articles providing noval insights to molecular mechanisms for tumorigenesis and metastasis, as well as the latest progress related to new biomarkers, therapeutic targets and development of new treatment strategies that will contribute to improved therapeutic efficacy and prognosis for cancer patients.

Prof. Dr. Lei Xue
Prof. Dr. Xiaolin Bi
Prof. Dr. Shian Wu
Prof. Dr. Xiaoping Zhang
Guest Editors

Manuscript Submission Information

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Keywords

  • cell death
  • cell proliferation and migration
  • oncogene and tumor suppressor genes
  • tumorigenesis, invasion and metastasis
  • tumor diagnosis and therapy
  • tumor-related signalling pathways

Published Papers (1 paper)

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Research

18 pages, 8258 KiB  
Article
Diane-35 and Metformin Induce Autophagy and Apoptosis in Polycystic Ovary Syndrome Women with Early-Stage Endometrial Carcinoma
by Yanjun Liu, Yang Wang, Dan Yao, Xing Chen, Feifei Zhang, Yi Feng and Xin Li
Genes 2022, 13(1), 131; https://doi.org/10.3390/genes13010131 - 12 Jan 2022
Cited by 2 | Viewed by 3331
Abstract
Objective: Women with polycystic ovary syndrome (PCOS) are at increased risk ofendometrial carcinoma (EC). Previous studies indicated that the combined therapy of Diane-35 and metformin significantly suppresses disease progression in PCOS patients with early EC; however, the mechanisms remain unclear. Methods: An established [...] Read more.
Objective: Women with polycystic ovary syndrome (PCOS) are at increased risk ofendometrial carcinoma (EC). Previous studies indicated that the combined therapy of Diane-35 and metformin significantly suppresses disease progression in PCOS patients with early EC; however, the mechanisms remain unclear. Methods: An established murine model of PCOS with early EC, clinical specimens, and human EC cells was used in this study. The levels of protein and mRNA were measured with Western blotting and RT-PCR, respectively. Cell proliferation was determined with MTT, colony formation, and flow cytometry. Proteins were analyzed with immunofluorescence and immunohistochemistry. Results: Diane-35 and metformin significantly inhibited proliferative activity and promoted apoptosis in EC cells. Additionally, cell autophagy was induced by the combined therapy. Quantitive PCR revealed that Diane-35 and metformin decreased androgen receptor (AR) expression but elevated GLUT4 expression. AR was found to repress GLUT4 expression by binding to the promoter of GLUT4. Moreover, the combined treatment mediated the onset of cellular autophagy by regulating the mTORC pathway via the suppression of IGF-1 and inhibited the development of EC by the activation of the PI3K/mTORC pathway. Conclusion: The results and previous clinical evidence support the use of Diane-35 and metformin combination therapy for patients with PCOS and early EC. Full article
(This article belongs to the Special Issue Molecular and Genetic Mechanism of Tumorigenesis)
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