Loss of TIPE3 reduced the proliferation, survival and migration of lung cancer cells through inactivation of Akt/mTOR, NF-κB, STAT-3 signaling cascade

Life Sciences ◽  
2022 ◽  
pp. 120332
Author(s):  
Devivasha Bordoloi ◽  
Choudhary Harsha ◽  
Ganesan Padmavathi ◽  
Kishore Banik ◽  
Bethsebie Lalduhsaki Sailo ◽  
...  
2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.


Tumor Biology ◽  
2017 ◽  
Vol 39 (10) ◽  
pp. 101042831771244 ◽  
Author(s):  
Dongjie Yao ◽  
Hujun Cui ◽  
Shufen Zhou ◽  
Ling Guo

2021 ◽  
Vol 21 (3) ◽  
Author(s):  
Chen-Chu Lin ◽  
Tsung-Ying Yang ◽  
Hseuh-Ju Lu ◽  
Chen-Kai Wan ◽  
Shih-Lan Hsu ◽  
...  

2020 ◽  
Vol 40 (5) ◽  
pp. 2583-2589
Author(s):  
NICHARAT SRIRATANASAK ◽  
NONGYAO NONPANYA ◽  
WORAWAT WATTANATHANA ◽  
PITHI CHANVORACHOTE

Toxins ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 367
Author(s):  
Peng Zhang ◽  
Yujie Yan ◽  
Junting Wang ◽  
Xiaoping Dong ◽  
Gaihua Zhang ◽  
...  

Spider venom has been found to show its anticancer activity in a variety of human malignancies, including lung cancer. In this study, we investigated the anti-cancer peptide toxin LVTX-8, with linear amphipathic alpha-helical conformation, designed and synthesized from the cDNA library of spider Lycosa vittata. Multiple cellular methods, such as CCK-8 assay, flow cytometry, colony formation assay, Transwell invasion and migration assay, were performed to detect peptide-induced cell growth inhibition and anti-metastasis in lung cancer cells. Our results demonstrated that LVTX-8 displayed strong cytotoxicity and anti-metastasis towards lung cancer in vitro. Furthermore, LVTX-8 could suppress the growth and metastasis of lung cancer cells (A549 and H460) in nude mouse models. Transcriptomics, integrated with multiple bioinformatics analysis, suggested that the molecular basis of the LVTX-8-mediated inhibition of cancer cell growth and metastasis manifested in two aspects: Firstly, it could restrain the activity of cancer cell division and migration through the functional pathways, including “p53 hypoxia pathway” and “integrin signaling”. Secondly, it could regulate the expression level of apoptotic-related proteins, which may account for programmed apoptosis of cancer cells. Taken together, as an anticancer peptide with high efficiency and acceptable specificity, LVTX-8 may become a potential precursor of a therapeutic agent for lung cancer in the future.


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