Retracted : microRNA‐383 suppresses the PI3K‐AKT‐MTOR signaling pathway to inhibit development of cervical cancer via down‐regulating PARP2

2018 ◽  
Vol 119 (7) ◽  
pp. 5243-5252 ◽  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

Overexpression of LINC00037 represses cervical cancer progression by activating mTOR signaling pathway

2019 ◽  
Vol 234 (8) ◽  
pp. 13353-13360
Author(s):  
Li‐Yun Yuan ◽  
Xiaomin Qin ◽  
Lin Li ◽  
Jinting Zhou ◽  
Min Zhou ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals SPAG5 upregulation predicts poor prognosis in cervical cancer patients and alters sensitivity to taxol treatment via the mTOR signaling pathway

2014 ◽  
Vol 5 (5) ◽  
pp. e1247-e1247 ◽  
Author(s):  
L-J Yuan ◽  
J-D Li ◽  
L Zhang ◽  
J-H Wang ◽  
T Wan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Patients ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Cell Function ◽  
Disease Free Survival ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway

Abstract Previously, we found that sperm-associated antigen 5 (SPAG5) was upregulated in pelvic lymph node metastasis–positive cervical cancer. The aim of this study is to examine the role of SPAG5 in the proliferation and tumorigenicity of cervical cancer and its clinical significance in tumor progression. In our study, SPAG5 expression in cervical cancer patients was detected using quantitative real-time polymerase chain reaction, western blotting, and immunohistochemistry; cervical cancer cell function with downregulated SPAG5 in vitro was explored using tetrazolium assay, flow cytometry, and colony formation and Transwell assays. SPAG5 was upregulated in tumor tissue compared with paired adjacent noncancerous tissues; SPAG5 upregulation in tumor tissues indicated poor disease-free survival, which was also an independent prognostic indicator for cervical cancer patients. In vitro study demonstrated that SPAG5 downregulation inhibited cell proliferation and growth significantly by G2/M arrest and induction of apoptosis, and hindered cell migration and invasion. Under SPAG5 downregulation, the sensitivity of cervical cancer cells differed according to taxol dose, which correlated with mammalian target of rapamycin (mTOR) signaling pathway activity. In general, SPAG5 upregulation relates to poor prognosis in cervical cancer patients, and SPAG5 is a regulator of mTOR activity during taxol treatment in cervical cancer.

MiR-21 modulates radiosensitivity of cervical cancer through inhibiting autophagy via the PTEN/Akt/HIF-1α feedback loop and the Akt-mTOR signaling pathway

Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12161-12168 ◽  
Author(s):  
Lili Song ◽  
Shikai Liu ◽  
Liang Zhang ◽  
Hairong Yao ◽  
Fangyuan Gao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Feedback Loop ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

Therapeutic effects of antibiotic drug mefloquine against cervical cancer through impairing mitochondrial function and inhibiting mTOR pathway

2017 ◽  
Vol 95 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Hui Li ◽  
Shun Jiao ◽  
Xin Li ◽  
Hasina Banu ◽  
Shreejana Hamal ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Colony Formation ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Antibiotic Drug ◽  
Cervical Cancer Cells

Targeting mitochondria is an attractive strategy for cancer therapy due to the essential roles of mitochondria in cancer cell energy metabolism. In this study, we show that mefloquine, an antibiotic drug, effectively targets cervical cancer cells through impairing mitochondrial function. Mefloquine dose-dependently induces apoptosis and inhibits proliferation and anchorage-independent colony formation of multiple cervical cancer cell lines. Mefloquine alone inhibits cervical tumor growth in vivo and its combination with paclitaxel is synergistic in inhibiting tumor growth. Mechanistically, mefloquine inhibits mitochondrial function via inhibiting mitochondrial respiration, decreasing membrane potential, increasing ROS generation, and decreasing ATP level. We further show that mefloquine suppresses activation of mTOR signaling pathway in HeLa cells. However, the inhibitory effects of mefloquine on survival, colony formation, and ATP are abolished in mitochondrial respiration-deficient HeLa ρ0 cells, demonstrating that mefloquine acts on cervical cancer cells via targeting mitochondrial respiration. Inhibition of mTOR signaling pathway by mefloquine was also reversed in HeLa ρ0 cells, suggesting deactivation of mTOR pathway as a consequence of mitochondria function disruption. Our work suggests that mefloquine is a potential candidate for cervical cancer treatment. Our work also highlights the therapeutic value of anti-mitochondria and establishes the association of mitochondrial function and the activation of mTOR signaling pathway in cervical cancer cells.

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