Sin1 promotes proliferation and invasion of prostate cancer cells by modulating mTORC2-AKT and AR signaling cascades

Huang, Yunchuanxiang; Feng, Guanying; Cai, Jingshu; Peng, Qian; Yang, Zhenglin; Yan, Chunhong; Lü, Yang; Wang, Ziyan

doi:10.1016/j.lfs.2020.117449

Cited by 9 publications

(11 citation statements)

References 46 publications

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“…Moreover, prohibitin (PHB), CDK18, and target of rapamycin complex 2 subunit (MAPKAP1) also play important roles in apoptosis, autophagy, and cell proliferation. [69][70][71][72] In our study, these proteins were also identified in the precipitation complex of HBV_circ_1-proteins; therefore, whether HBV-related HCC is promoted by interaction of HBV_circ_1 with PHB, CDK18, and MAPKAP1 remains to be investigated.…”

Section: Discussionmentioning

confidence: 69%

Hepatocellular carcinoma progression mediated by hepatitis B virus-encoded circRNA HBV_circ_1 through interaction with CDK1

Zhu

Liang

Pan

et al. 2021

Molecular Therapy - Nucleic Acids

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Hepatitis B virus (HBV) produces circular RNA (circRNA), whose functions have not yet been clearly elucidated. In this study, a novel circRNA HBV_circ_1 produced by HBV was identified in HBV-positive HepG2.2.15 cells and HBV-related hepatocellular carcinoma (HCC) tissue (HCCT). Microarray analysis of 68 HCCT samples showed that HBV_circ_1 abundance was significantly higher than that in paracancerous tissues. In addition, survival rate of HBV_circ_1-positive patients was significantly lower compared with HBV_circ_1-negative patients. Transient expression indicated that HBV_circ_1 enhanced cell proliferation, migration, and invasion and inhibited apoptosis in vitro . Furthermore, ectopical HBV_circ_1 expression increased tumor size in vivo . HBV_circ_1 was confirmed to interact with cyclin-dependent kinase 1 (CDK1) to regulate cell proliferation. These results suggest that HCC progression may be promoted by interaction of HBV_circ_1 with CDK1. Our data not only showed a novel clue to understand carcinogenesis and progress of HBV-related HCC but also provided a new target for the development of therapeutic drugs.

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Section: Discussionmentioning

confidence: 69%

Hepatocellular carcinoma progression mediated by hepatitis B virus-encoded circRNA HBV_circ_1 through interaction with CDK1

Zhu

Liang

Pan

et al. 2021

Molecular Therapy - Nucleic Acids

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“…FAK signaling pathway was activated in multiple human cancers including prostate cancer [ 16 ]. AKT is activated by FAK stimulation, regulating cell migration and invasion [ 23 ]. Accumulating evidence suggests that the activation of FAK/AKT signaling promotes tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

RAB11A Promotes Cell Malignant Progression and Tumor Formation of Prostate Cancer via Activating FAK/AKT Signaling Pathway

Chen

Wang

2023

Evidence-Based Complementary and Alternative Medicine

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Background. RAB11A, a member of the GTPase family, acts as a regulator in diverse cancers development. The dysregulation of the FAK/AKT signaling pathway is mainly related to tumorigenesis. This study aimed to investigate the possible effect of RAB11A in prostate cancer and further explore the potential mechanisms. Results. In this study, we illustrated the tumor-promoting effects of RAB11A based on in vivo and in vitro experiments. RAB11A expression was upregulated in prostate cancer cells. RAB11A knockdown decreased the prostate cancer cell proliferation, migration, and invasion. RAB11A also induced the epithelial-mesenchymal transition. PF562271 suppressed the malignant characteristics of prostate cancer cells caused by RAB11A knockdown. Furthermore, the interference of RAB11A reduced the tumor growth and the protein levels of p-FAK/FAK and p-AKT/AKT in vivo. Conclusion. RAB11A promotes cell malignant progression and tumor formation in prostate cancer via activating FAK/AKT signaling pathway.

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“…As a cancer suppressor gene, PTEN mutation is widely observed in multiple cancers, such as breast, bladder, and prostate cancer [19][20][21]. Importantly, SP1 is an upstream regulator of PTEN and represses PTEN transcription [22].…”

Section: Discussionmentioning

confidence: 99%

The Role of Specificity Protein 1 (SP1) in Bladder Cancer Progression through PTEN-Mediated AKT/mTOR Pathway

Chen

2023

Urol Int

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Introduction: The aim of the study was to investigate the potential mechanism of specificity protein 1 (SP1) in bladder cancer progression through the PTEN-mediated AKT/mTOR pathway. Methods: Human bladder cancer cell lines (HT-1197, HT-1376, and T24) and normal ureteral epithelial cell line SV-HUC-1 were used. SP1 expression was detected via quantitative real-time PCR and Western blotting. Cell viability, migration, invasion, and apoptosis were assessed using CCK-8, transwell, and flow cytometry assays, respectively. The involvement of the PTEN-mediated AKT/mTOR pathway was evaluated by Western blot. A mouse xenograft model was built, and immunohistochemical staining was applied to visualize SP1 and Ki67 expression in tumor tissues. Results: SP1 was overexpressed in bladder cancer cells. SP1 knockdown inhibited viability, migration, and invasion and promoted apoptosis in bladder cancer cells. PTEN intervention increased cell viability, migration, and invasion and decreased apoptosis, which was reversed by SP1 knockdown. The activation of the AKT/mTOR pathway resulting from PTEN knockdown was attenuated by SP1 knockdown. In vivo results showed that SP1 knockdown suppressed tumor growth, increased PTEN expression, and decreased AKT/mTOR pathway-related protein levels. Conclusion: SP1 promotes bladder cancer progression by inhibiting the PTEN-mediated AKT/mTOR pathway. Targeting SP1 may be a potential therapeutic strategy for treating bladder cancer.

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Sin1 promotes proliferation and invasion of prostate cancer cells by modulating mTORC2-AKT and AR signaling cascades

Cited by 9 publications

References 46 publications

Hepatocellular carcinoma progression mediated by hepatitis B virus-encoded circRNA HBV_circ_1 through interaction with CDK1

Hepatocellular carcinoma progression mediated by hepatitis B virus-encoded circRNA HBV_circ_1 through interaction with CDK1

RAB11A Promotes Cell Malignant Progression and Tumor Formation of Prostate Cancer via Activating FAK/AKT Signaling Pathway

The Role of Specificity Protein 1 (SP1) in Bladder Cancer Progression through PTEN-Mediated AKT/mTOR Pathway

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