To be or not to be: navigating the influence of MicroRNAs on cervical cancer cell death

被引：0

作者：

Mohammad Taghizadieh ^{[1
]}

Masoumeh Kalantari ^{[2
]}

Roksana Bakhshali ^{[3
]}

Sepehr Kobravi ^{[4
]}

Shayan Khalilollah ^{[5
]}

Hossein Bannazadeh Baghi ^{[6
]}

Mobina Bayat ^{[6
]}

Javid Sadri Nahand ^{[6
]}

Reza Akhavan-Sigari ^{[7
]}

机构：

[1] Department of Pathology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz

[2] Department of Biology, Tehran University of health Sciences, Tehran

[3] Omid Cancer Center, Ahvaz

[4] Department of Oral & Maxillofacial Surgery, Faculty of Dentistry, Tehran Medical Sciences Branch, Islamic Azad University, Tehran

[5] Department of Neurosurgery, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran

[6] Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz

[7] Department of Neurosurgery, University Medical Center Tuebingen, Tuebingen

[8] Department of Health Care Management and Clinical Research, Collegium Humanum Warsaw Management University, Warsaw

来源：

Cancer Cell International | / 25卷 / 1期

关键词：

Apoptosis; Autophagy; Cervical cancer; Ferroptosis; MicroRNAs; Pyroptosis;

D O I：

10.1186/s12935-025-03786-y

中图分类号：

学科分类号：

摘要：

With all diagnostic and therapeutic advances, such as surgery, radiation- and chemo-therapy, cervical cancer (CC) is still ranked fourth among the most frequent cancers in women globally. New biomarkers and therapeutic targets are warranted to be discovered for the early detection, treatment, and prognosis of CC. As component of the non-coding RNA’s family, microRNAs (miRNAs) participate in several cellular functions such as cell proliferation, gene expression, many signaling cascades, apoptosis, angiogenesis, etc. MiRNAs can suppress or induce programmed cell death (PCD) pathways by altering their regulatory genes. Besides, abnormal expression of miRNAs weakens or promotes various signaling pathways associated with PCD, resulting in the development of human diseases such as CC. For that reason, understanding the effects that miRNAs exert on the various modes of tumor PCD, and evaluating the potential of miRNAs to serve as targets for induction of cell death and reappearance of chemotherapy. The current study aims to define the effect that miRNAs exert on cell apoptosis, autophagy, pyroptosis, ferroptosis, and anoikis in cervical cancer to investigate possible targets for cervical cancer therapy. Manipulating the PCD pathways by miRNAs could be considered a primary therapeutic strategy for cervical cancer. © The Author(s) 2025.

引用

共 167 条

[61] Li J., Qiu M., An Y., Huang J., Gong C., miR-7-5p acts as a tumor suppressor in bladder cancer by regulating the Hedgehog pathway factor Gli3, Biochem Biophys Res Commun, 503, 3, pp. 2101-2107, (2018)
[62] Zhang J., Li S., Li Y., Liu H., Zhang Y., Zhang Q., miRNA-218 regulates the proliferation and apoptosis of cervical cancer cells via targeting Gli3, Exp Ther Med, 16, 3, pp. 2433-2441, (2018)
[63] He Y., Sun M.M., Zhang G.G., Yang J., Chen K.S., Xu W.W., Et al., Targeting PI3K/Akt signal transduction for cancer therapy, Signal Transduct Target Therapy, 6, 1, (2021)
[64] Parsons J.T., Focal adhesion kinase: the first ten years, J Cell Sci, 116, 8, pp. 1409-1416, (2003)
[65] Mitra S.K., Hanson D.A., Schlaepfer D.D., Focal adhesion kinase: in command and control of cell motility, Nat Rev Mol Cell Biol, 6, 1, pp. 56-68, (2005)
[66] Sonoda Y., Watanabe S., Matsumoto Y., Aizu-Yokota E., Kasahara T., FAK is the upstream signal protein of the phosphatidylinositol 3-kinase-Akt survival pathway in hydrogen peroxide-induced apoptosis of a human glioblastoma cell line, J Biol Chem, 274, 15, pp. 10566-10570, (1999)
[67] Sonoda Y., Matsumoto Y., Funakoshi M., Yamamoto D., Hanks S.K., Kasahara T., Anti-apoptotic role of focal adhesion kinase (FAK). Induction of inhibitor-of-apoptosis proteins and apoptosis suppression by the overexpression of FAK in a human leukemic cell line, HL-60, J Biol Chem, 275, 21, pp. 16309-16315, (2000)
[68] Kasahara T., Koguchi E., Funakoshi M., Aizu-Yokota E., Sonoda Y., Antiapoptotic action of focal adhesion kinase (FAK) against ionizing radiation, Antioxid Redox Signal, 4, 3, pp. 491-499, (2002)
[69] Yamamoto D., Sonoda Y., Hasegawa M., Funakoshi-Tago M., Aizu-Yokota E., Kasahara T., FAK overexpression upregulates Cyclin D3 and enhances cell proliferation via the PKC and PI3-kinase-Akt pathways, Cell Signal, 15, 6, pp. 575-583, (2003)
[70] Reif S., Lang A., Lindquist J.N., Yata Y., Gabele E., Scanga A., Et al., The role of focal adhesion kinase-phosphatidylinositol 3-kinase-akt signaling in hepatic stellate cell proliferation and type I collagen expression, J Biol Chem, 278, 10, pp. 8083-8090, (2003)

← 2 3 4 5 6 7 8 9 10 11 →