Glycogen synthase kinase‐3β inactivation promotes cervical cancer progression, invasion, and drug resistance

Nath, Nidhi; Rana, Ajay; Nagini, Siddavaram; Mishra, Rajakishore

doi:10.1002/bab.2258

Cited by 4 publications

(1 citation statement)

References 41 publications

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“…On the other hand, Gepia database revealed that in CC tumor tissues, RSF-1 expression is positively correlated with VEGFA, AKT1 and GSK3β expression. AKT/ GSK3β pathway was widely involved in cell survival and cisplatin resistance in cancers [25][26][27][28]. Vascular endothelial growth factor A(VEGFA) is a key factor associated with angiogenesis in tumors 29 .…”

Section: Introductionmentioning

confidence: 99%

linc00958/miR-185-5p/RSF-1 modulates cisplatin resistance and angiogenesis through AKT1/GSK3β/VEGFA pathway in cervical cancer

Tian

Cheng

Kong

et al. 2022

Reprod Biol Endocrinol

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Background Chemoresistance is one of the major obstacles that lead to poor prognosis in cervical cancer. linc00958 was reported to be an oncogene in cervical cancer. However, its role in mediating chemoresistance remains to be revealed. Purpose To explore the regulatory mechanisms of linc00958 in cisplatin-resistant cervical cancer cells and further validate in xenograft mice. Methods Online bioinformatic tools were used to conduct the pre-investigation of linc00958/miR-185-5p/RSF-1 and predict the associations between RSF-1 and AKT1/GSK3β/VEGFA in cervical cancer. RT-qPCR measured the RNA expression levels of linc00958/miR-185-5p/RSF-1 in SiHa and SiHa/DDP. Cell survival rates were evaluated by CCK8 methods after cells were exposed to differential concentrations of DDP. Dual-luciferase reporter methods were used to measure luciferase activity. Western blot measured RSF-1 protein and phosphorylated changes of AKT1/GSK3β. Immunofluorescence was employed to observe VEGFA secretion in vitro. Tube formation was applied to evaluate the in-vitro changes of angiogenesis. The SiHa/DDP cells stably transfected with pLKO-sh-NC or pLKO-sh-linc00958 plasmids, were injected into mice, establishing xenograft models. The changes in mice weight and tumor volumes were recorded. H&E staining and Immunohistochemistry (IHC) method was further performed. Results linc00958 expression was higher in SiHa/DDP cells. High linc00958 expression was associated with low overall survival. In SiHa/DDP cells linc00958/miR-185-5p/RSF-1 axis inhibited the cellular resistance to cisplatin and suppressed VEGFA and the tube formation through AKT1/GSK3β/VEGFA pathway. The knockdown of linc00958 inhibited RSF-1 and Ki67, curbing tumor growth; it also inhibited VEGFA and CD34, decreasing angiogenesis in mice. Conclusion linc00958/miR-185-5p/RSF-1 modulates cisplatin resistance and angiogenesis through AKT1/GSK3β/VEGFA pathway in cervical cancer.

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Section: Introductionmentioning

confidence: 99%

linc00958/miR-185-5p/RSF-1 modulates cisplatin resistance and angiogenesis through AKT1/GSK3β/VEGFA pathway in cervical cancer

Tian

Cheng

Kong

et al. 2022

Reprod Biol Endocrinol

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Therapeutic role of microRNAs in management of head and neck cancer

Tiwari,

Kumar,

Mishra

2024

Diagnostic, Prognostic, and Therapeutic Role of MicroRNAs in Head and Neck Cancer

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Crosstalk between cell fate and survival pathways during uterine cervical carcinoma progression: a molecular and clinical perspective

Samadder¹,

Paul²,

De³

2023

J Cancer Metastasis Treat

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The development of uterine cervical cancer is primarily attributed to infection by high-risk human papillomaviruses (HR-HPVs). E5, E6 and E7, the three early oncoproteins of HR-HPVs, have been implicated in initiation and progression of cervical cancer. The intricate molecular mechanisms that orchestrate aberrant cellular transformations to establish carcinoma of the cervical epithelium following viral infections are poorly understood. Here, we discuss how deregulation of three major cell fate regulatory pathways, Hedgehog, Wnt and Notch, and cell survival strategies involving EGFR signaling and G1/S checkpoint contribute towards cervical cancer development and progression. Further exploration of protein interaction database has revealed several genes that are involved in cervical cancer initiation and progression, and the two crucial "driver” genes, MYC and CTNNB1 (β-catenin), have been identified as major players in protein-protein interaction network. GSK3β emerged as the key mediator of crosstalk between Hedgehog, Wnt and Notch signaling pathways. GSK3β regulates cytoplasmic stabilization and nuclear translocation of β-catenin, which further impacts the expression of MYC, critical for cell cycle progression. Collectively, our analyses suggest that combinatorial therapeutic targeting of these proteins may be more effective in blocking cervical cancer initiation and progression.

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Glycogen synthase kinase‐3β inactivation promotes cervical cancer progression, invasion, and drug resistance

Cited by 4 publications

References 41 publications

linc00958/miR-185-5p/RSF-1 modulates cisplatin resistance and angiogenesis through AKT1/GSK3β/VEGFA pathway in cervical cancer

linc00958/miR-185-5p/RSF-1 modulates cisplatin resistance and angiogenesis through AKT1/GSK3β/VEGFA pathway in cervical cancer

Therapeutic role of microRNAs in management of head and neck cancer

Crosstalk between cell fate and survival pathways during uterine cervical carcinoma progression: a molecular and clinical perspective

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