RRS1 Promotes Retinoblastoma Cell Proliferation and Invasion via Activating the AKT/mTOR Signaling Pathway

Ribosome biogenesis regulatory protein homolog (RRS1) is a protein required for ribosome biogenesis. Recent studies have identified an oncogenic role of RRS1 in some cancers, whereas the involvement of RRS1 in retinoblastoma (RB) remains to be determined. In this study, we aimed to explore the role of RRS1 in RB. We found that the expression of RRS1 was increased in RB tissues and cells. Lentivirus-mediated RRS1 overexpression promoted the proliferation, growth, and invasion of RB cells. Opposite results were found in RRS1 knockdown cells. In addition, RRS1 silencing induced cell cycle arrest at the G1 phase and apoptosis in RB cells, while RRS1 ectopic expression exhibited the opposite effect. At the molecular level, RRS1 activated the AKT/mTOR signaling pathway, inhibition of which largely blunted the proliferation, growth, and invasion of RB cells. Our study suggests that RRS1 functions as an oncogene in RB through activating the AKT/mTOR signaling pathway.

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ANLN promotes carcinogenesis in oral cancer by regulating the PI3K/mTOR signaling pathway

Head & Face Medicine ◽

10.1186/s13005-021-00269-z ◽

2021 ◽

Vol 17 (1) ◽

Author(s):

Bing Wang ◽

Xiao-li Zhang ◽

Chen-xi Li ◽

Ning-ning Liu ◽

Min Hu ◽

...

Keyword(s):

Oral Cancer ◽

Signaling Pathway ◽

Cell Cycle Progression ◽

Mtor Signaling ◽

Mtor Signaling Pathway ◽

Cell Behaviors ◽

Rnai Technology ◽

Tumor Tissues ◽

Pi3k Signaling Pathway

Abstract Background Oral cancer is a malignant disease that threatenshuman life and greatly reducespatientquality of life. ANLN was reported to promote the progression of cancer. This study aims to investigate the role of ANLNin oral cancer and the underlying molecular mechanism. Methods ANLN expression was downregulated by RNAi technology. The effect of ANLN on cell behaviors, including proliferation, cell cycle progression, invasion, and apoptosis, was detected. Western blotting analysis was used to explore the mechanism by whichANLN functions in oral cancer. Results Data from TCGA database showed that ANLN was expressed at significantly higher levels in tumor tissues thanin normal control tissues. Patients with higher ANLN expression exhibitedshorter survivaltimes. ANLN was alsoabundantly expressedin the cancer cell lines CAL27 and HN30. When ANLN was knocked down in CAL27 and HN30 cells, cell proliferation and colony formation weredecreased. The cell invasion ability was also inhibited. However, the cell apoptosis rate was increased. In addition, the levels of critical members of the PI3K signaling pathway, includingPI3K, mTOR, Akt, and PDK-1, were significantlyreducedafter ANLN was knocked down in CAL27 cells. Conclusions ANLN contributes to oral cancerprogressionand affects activation ofthe PI3K/mTOR signaling pathway. This study providesa new potential targetfor drug development and treatment in oral cancer.

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Inhibition of Prostate Cancer DU-145 Cells Proliferation by Anthopleura anjunae Oligopeptide (YVPGP) via PI3K/AKT/mTOR Signaling Pathway

Marine Drugs ◽

10.3390/md16090325 ◽

2018 ◽

Vol 16 (9) ◽

pp. 325 ◽

Cited By ~ 16

Author(s):

Xiaojuan Li ◽

Yunping Tang ◽

Fangmiao Yu ◽

Yu Sun ◽

Fangfang Huang ◽

...

Keyword(s):

Prostate Cancer ◽

Signaling Pathway ◽

Caspase 3 ◽

Mtor Signaling ◽

Mtor Signaling Pathway ◽

Nude Mouse Model ◽

Dose Dependent

We investigated the antitumor mechanism of Anthopleura anjunae oligopeptide (AAP-H, YVPGP) in prostate cancer DU-145 cells in vitro and in vivo. Results indicated that AAP-H was nontoxic and exhibited antitumor activities. Cell cycle analysis indicated that AAP-H may arrest DU-145 cells in the S phase. The role of the phosphatidylinositol 3-kinase/protein kinase B/mammalian rapamycin target protein (PI3K/AKT/mTOR) signaling pathway in the antitumor mechanism of APP-H was investigated. Results showed that AAP-H treatment led to dose-dependent reduction in the levels of p-AKT (Ser473), p-PI3K (p85), and p-mTOR (Ser2448), whereas t-AKT and t-PI3K levels remained unaltered compared to the untreated DU-145 cells. Inhibition of PI3K/AKT/mTOR signaling pathway in the DU-145 cells by employing inhibitor LY294002 (10 μM) or rapamycin (20 nM) effectively attenuated AAP-H-induced phosphorylation of AKT and mTOR. At the same time, inhibitor addition further elevated AAP-H-induced cleaved-caspase-3 levels. Furthermore, the effect of AAP-H on tumor growth and the role of the PI3K/AKT/mTOR signaling pathway in nude mouse model were also investigated. Immunohistochemical analysis showed that activated AKT, PI3K, and mTOR levels were reduced in DU-145 xenografts. Western blotting showed that AAP-H treatment resulted in dose-dependent reduction in p-AKT (Ser473), p-PI3K (p85), and p-mTOR (Ser2448) levels, whereas t-AKT and t-PI3K levels remained unaltered. Similarly, Bcl-xL levels decreased, whereas that of Bax increased after AAP-H treatment. AAP-H also increased initiator (caspase 8 and 9) and executor caspase (caspase 3 and 7) levels. Therefore, the antitumor mechanism of APP-H on DU-145 cells may involve regulation of the PI3K/AKT/mTOR signaling pathway, which eventually promotes apoptosis via mitochondrial and death receptor pathways. Thus, the hydrophobic oligopeptide (YVPGP) can be developed as an adjuvant for the prevention or treatment of prostate cancer in the future.

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Role of the Akt/mTOR signaling pathway in human papillomavirus-associated nasal and sinonasal inverted papilloma

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmx108 ◽

2017 ◽

Vol 49 (12) ◽

pp. 1067-1074 ◽

Cited By ~ 5

Author(s):

Yongliang Liu ◽

Lihua Duan ◽

Jie Tian ◽

Daoliang Song ◽

Min Zhang ◽

...

Keyword(s):

Human Papillomavirus ◽

Signaling Pathway ◽

Mtor Signaling ◽

Inverted Papilloma ◽

Mtor Signaling Pathway ◽

Sinonasal Inverted Papilloma

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Cell Cycle Arrest of Extract from Artemisia annua Linné. Via Akt-mTOR Signaling Pathway in HCT116 Colon Cancer Cells

KSBB Journal ◽

10.7841/ksbbj.2015.30.5.223 ◽

2015 ◽

Vol 30 (5) ◽

pp. 223-229 ◽

Cited By ~ 3

Author(s):

Bo Min Kim ◽

Guen Tae Kim ◽

Eun Gyeong Lim ◽

Eun Ji Kim ◽

Sang Yong Kim ◽

...

Keyword(s):

Cell Cycle ◽

Colon Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Signaling Pathway ◽

Artemisia Annua ◽

Mtor Signaling ◽

Colon Cancer Cells ◽

Mtor Signaling Pathway ◽

Cycle Arrest

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MicroRNA-1271-5p inhibits the tumorigenesis of ovarian cancer through targeting E2F5 and negatively regulates the mTOR signaling pathway

10.21203/rs.3.rs-17270/v1 ◽

2020 ◽

Author(s):

Qin Li ◽

Junyu Shi ◽

Xiaoli Xu

Keyword(s):

Ovarian Cancer ◽

Signaling Pathway ◽

Poor Prognosis ◽

Mtor Signaling ◽

Luciferase Assay ◽

Migration And Invasion ◽

Mtor Signaling Pathway ◽

Direct Target ◽

The Relationship

Abstract Background: MicroRNA-1271-5p (miR-1271-5p) has been reported to participate in the progression of many human cancers. However, the role of miR-1271-5p still remains unclear in ovarian cancer (OC). Therefore, we explored the effect of miR-1271-5p on the development of OC in present study. Methods: We measured the miR-1271-5p expression via the qRT-PCR assay. Then the function of miR-1271-5p was analyzed through MTT and Transwell assays. The relationship among miR-1271-5p and E2F5 was verified by dual luciferase assay. The protein expression levels were examined through western blot.Results: MiR-1271-5p was downregulated in OC tissues which predicted poor prognosis of OC patients. Moreover, E2F5 was a direct target of miR-1271-5p in OC. And miR-1271-5p suppressed cell proliferation, migration and invasion in OC through targeting E2F5. Furthermore, E2F5 was upregulated in OC tissues which predicted poor prognosis of OC patients. Besides that, miR-1271-5p suppressed EMT and mTOR pathway in OC. Conclusion: MiR-1271-5p inhibited the tumorigenesis of OC through targeting E2F5 and negatively regulated the mTOR signaling pathway.

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