Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non‑small cell lung cancer via the regulation of epithelial‑to‑mesenchymal transition

Xu, Xiang; Zhu, Huarui; Yang, Minglei; Zheng, Enkuo; Zhou, Ye; Ni, Junjun; Li, Rui; Yang, Zhenhua; He, Tao; Zhao, Guofang

doi:10.3892/etm.2019.8358

Cited by 7 publications

(6 citation statements)

References 30 publications

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“…TIPRL expression was increased in NSCLC tissues in comparison to normal tissues, and TIPRL could contribute to autophagy so as to facilitate NSCLC development through the eukaryotic initiation factor 2α (eIF2α)-Activating Transcription Factor 4 (ATF4) pathway [ 23 ]. In addition, TIPRL was found to correlated with lower overall survival rate of NSCLC patients; TIPRL knockdown suppressed NSCLC metastasis, indicating that TIPRL acted as an oncogene in NSCLC [ 36 ]. Similarly, our data also showed that TIPRL was upregulated in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Zhang

Cheng

et al. 2021

Cancer Cell Int

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Background Non-small cell lung cancer (NSCLC) is a threat to human health. Circular RNAs (circRNAs) have been proved to function in NSCLC development. In this study, the role of circRNA hsa_circ_0010235 in NSCLC progression and the possible molecular mechanism were explored. Methods Expression of hsa_circ_0010235, miRNA (miR)-433-3p and TOR signaling pathway regulator-like (TIPRL) was examined by quantitative real-time PCR (qRT-PCR). Cell viability and clonogenicity were detected by cell counting kit-8 (CCK-8) assay and colony formation assay, respectively. Flow cytometry was performed to monitor cell apoptosis and cell cycle distribution. Western blot assay was employed to evaluate the protein levels of TIPRL, light chain 3 (LC3)-II/I and p62. Cell metastasis was assessed by Transwell and wound healing assays. The targeted relationship between miR-433-3p and hsa_circ_0010235 or TIPRL was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Furthermore, the role of hsa_circ_0010235 in vivo was investigated by xenograft assay. Results Hsa_circ_0010235 and TIPRL were highly expressed in NSCLC tissues and cells, while miR-433-3p was downregulated. Depletion of hsa_circ_0010235 or gain of miR-433-3p repressed proliferation and autophagy but promoted apoptosis in NSCLC cells. Hsa_circ_0010235 sponged miR-433-3p to upregulate TIPRL expression, so as to affect NSCLC development. Hsa_circ_0010235 knockdown also blocked tumor growth in vivo. Conclusion Hsa_circ_0010235 knockdown suppressed NSCLC progression by regulating miR-433-3p/TIPRL axis, affording a novel mechanism of NSCLC progression.

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Section: Discussionmentioning

confidence: 99%

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Zhang

Cheng

et al. 2021

Cancer Cell Int

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“…Using the same model, Zheng revealed that 160 mg/kg baicalin administration significantly alleviated kidney damage, metabolic disorders and renal fibrosis by anti-inflammatory and anti-oxidative stress mechanisms. Zheng’s results suggested that baicalin inhibits inflammation through the NF-κB signalling pathway, blocks extracellular matrix accumulation through the TGF-β/Smad3 pathway, and regulates cell proliferation via the insulin-like growth factor (IGF)-1/IGF-1 receptor/p38 mitogen-activated protein kinase (MAPK) pathway [ 48 ].…”

Section: Flavonoids For the Treatment Of Diabetic Nephropathymentioning

confidence: 99%

Flavonoids on diabetic nephropathy: advances and therapeutic opportunities

Xiaolin

et al. 2021

Chin Med

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With the advances in biomedical technologies, natural products have attracted substantial public attention in the area of drug discovery. Flavonoids are a class of active natural products with a wide range of pharmacological effects that are used for the treatment of several diseases, in particular chronic metabolic diseases. Diabetic nephropathy is a complication of diabetes with a particularly complicated pathological mechanism that affects at least 30% of diabetic patients and represents a great burden on public health. A large number of studies have shown that flavonoids can alleviate diabetic nephropathy. This review systematically summarizes the use of common flavonoids for the treatment of diabetic nephropathy. We found that flavonoids play a therapeutic role in diabetic nephropathy mainly by regulating oxidative stress and inflammation. Nrf-2/GSH, ROS production, HO-1, TGF-β1 and AGEs/RAGE are involved in the process of oxidative stress regulation. Quercetin, apigenin, baicalin, luteolin, hesperidin, genistein, proanthocyanidin and eriodictyol were found to be capable of alleviating oxidative stress related to the aforementioned factors. Regarding inflammatory responses, IL-1, IL-6β, TNF-α, SIRT1, NF-κB, and TGF-β1/smad are thought to be essential. Quercetin, kaempferol, myricetin, rutin, genistein, proanthocyanidin and eriodictyol were confirmed to influence the above targets. As a result, flavonoids promote podocyte autophagy and inhibit the overactivity of RAAS by suppressing the upstream oxidative stress and inflammatory pathways, ultimately alleviating DN. The above results indicate that flavonoids are promising drugs for the treatment of diabetic nephropathy. However, due to deficiencies in the effect of flavonoids on metabolic processes and their lack of structural stability in the body, further research is required to address these issues.

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“…Lung cancer diagnoses numbered 228,000 in the United States in 2019 with around 160,000 deaths ( 17 ), demonstrating the disease has a high incidence, high fatality rate, and a poor prognosis. Lung adenocarcinoma is the most prevalent form of NSCLC ( 18 , 19 ), and determining its mechanism of incidence, invasion, and metastasis.…”

Section: Discussionmentioning

confidence: 99%

PCK2 inhibits lung adenocarcinoma tumor cell immune escape through oxidative stress-induced senescence as a potential therapeutic target

Tang¹,

Sun²,

Cai³

2023

J Thorac Dis

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Background Our research aimed to better understand how phosphoenolpyruvate carboxykinase 2 ( PCK2 ) is linked to survival outcomes in lung cancer patients. Methods We confirmed PCK2 expression and its association with the outcome of lung cancer patients using The Cancer Genome Atlas (TCGA) database. PCK2 and immune cell connections were investigated using data from the Tumor IMmune Estimation Resource (TIMER) and TCGA repositories. We used the CancerSEA database to examine the links between PCK2 expression and the efficiency of lung adenocarcinomas, and a T-distributed Stochastic Neighbor Embedding (T-SNE) map was constructed to show the expression profile of PCK2 in single cells in TCGA lung adenocarcinoma samples. The potential mechanism of action was finally investigated using Gene Set Enrichment Analysis (GSEA) enrichment analysis, Gene Ontology (GO) pathway enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Results The expression of PCK was lower in lung adenocarcinoma tumor tissues than in paracancerous tissues. Patients with lung adenocarcinoma who expressed PCK2 at high levels fared better in overall survival (OS), disease-specific survival (DSS), and progression free interval (PFI). PCK2 was positively correlated with programmed cell death 1 ( PDCD1 ) expression, and its mutation rate in lung adenocarcinoma was 0.53%. CancerSEA research revealed that in lung adenocarcinoma, PCK2 was negatively correlated with epithelial-mesenchymal transition (EMT) and hypoxia. Gene ontology and KEGG enrichment analysis revealed PCK2 -coexpressed genes influenced the onset and progression of lung adenocarcinoma by modulating the activity of DNA-binding transcriptional activators, the specificity of RNA polymerase II, the interaction between neuroactive ligands and their receptors, and the cAMP signaling pathway. The prognosis for lung adenocarcinoma was shown to vary according to whether PCK2 was involved in the response to oxidative stress-induced senescence, gene silencing, cell cycle, and other biological processes. Conclusions An increased expression of PCK2 may be employed as a novel prognostic biomarker in patients with lung adenocarcinoma and has been shown to increase OS, DSS, and PFI. Improving the prognosis of lung adenocarcinoma by interference with PCK2 may be possible since it induces senescence through the oxidative stress response and blocks the immune escape of tumor cells. These results point to a probable target anticancer treatment development in lung adenocarcinoma.

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Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non‑small cell lung cancer via the regulation of epithelial‑to‑mesenchymal transition

Cited by 7 publications

References 30 publications

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Flavonoids on diabetic nephropathy: advances and therapeutic opportunities

PCK2 inhibits lung adenocarcinoma tumor cell immune escape through oxidative stress-induced senescence as a potential therapeutic target

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