RETRACTED ARTICLE: Testis developmental related gene 1 promotes non-small-cell lung cancer through the microRNA-214-5p/Krüppel-like factor 5 axis

Lü, Xudong; Zhao, Nian; Duan, Guangjun; Deng, Zhiyong; Lu, Yimin

doi:10.1080/21655979.2021.2012406

Cited by 6 publications

(3 citation statements)

References 48 publications

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“…Furthermore, α-Catulin has been reported to promote cancer stemness by antagonizing the WW domain-containing E3 ubiquitin protein ligase 1-mediated degradation of KLF5 in lung cancer ( 19 ). Testis development-related 1 serves a carcinogenic role in non-small cell lung cancer by targeting the microRNA (miR)-214-5p/KLF5 axis ( 20 ). KLF5-induced γ-butyrobetaine hydroxylase 1-antisense RNA 1 has been found to upregulate maternal embryonic leucine zipper kinase expression to activate focal adhesion kinase (FAK) signaling, by sponging miR-27a-5p, contributing to the malignant phenotype of non-small cell lung cancer ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

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Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Wang,

Yu,

et al. 2024

Exp Ther Med

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Lung cancer is a harmful type of malignancy and the leading cause of cancer-associated mortality. It is therefore imperative to develop novel drugs effective for treating this cancer. The Traditional Chinese Medicine compound Britannin has been previously reported to inhibit the development of certain cancers, such as pancreatic, breast and liver cancer. Moreover, Kruppel-like factor 5 (KLF5) has been identified an on oncogene in lung cancer. In the present study, the possible regulatory effects and underlying mechanism of Britannin in lung cancer were investigated. A549 and 16HBE cells were treated with different concentrations of Britannin. Subsequently, Cell counting kit-8, EdU staining and colony formation assays were used to detect the proliferative ability of these cells. Cell migration was detected by wound healing and Transwell assays, respectively. XF96 extracellular flux analyzer was used to analyze the extent of extracellular acidification and oxygen consumption rate in cells, whereas assay kits were used to detect glucose and lactic acid levels in the cell supernatant. The targeting effect between Britannin and the KLF5 protein was investigated using molecular docking technology. The protein expression levels of KLF5 in cells challenged with Britannin was detected by western blotting. Finally, overexpression of KLF5 in A549 cells was performed before cell proliferation, migration and the glycolysis rate were measured to explore the regulatory effects of Britannin. Britannin was found to inhibit the proliferation, migration and glycolysis of lung cancer cells, during which the protein expression levels of KLF5 were decreased. This suggests that Britannin regulated the expression of KLF5 in A549 cells. Overexpression of KLF5 reversed the inhibitory effects of Britannin on the proliferation, migration and glycolysis in lung cancer cells. In conclusion, these results suggest that Britannin can inhibit cell proliferation, migration and glycolysis by downregulating KLF5 expression in lung cancer cells.

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Section: Discussionmentioning

confidence: 99%

“…Research has revealed that abnormal expression of KLF5 is observed in a number of different types of cancer, such as breast, prostate and bladder cancer (17). Notably, increasing evidence has shown that KLF5 also exerts tumor-promoting activities in lung cancer (18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Wang,

Yu,

et al. 2024

Exp Ther Med

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“…In this article, miR-214-3p targeting of PTEN affected the downstream PI3K/AKT pathway, thereby regulating renal interstitial fibrosis and TGF β -induced EMT ( Figure 4 ). miR-214 was proven to upregulate the PI3K/AKT pathway by targeting PTEN, thereby protecting cells from damage induced by hypoxia/reoxygenation (H/R) and reducing myocardial damage induced by ischaemia/reperfusion (I/R) and cardiomyocyte apoptosis [ 44 , 45 ]. According to the results of this experiment, there may be a feedback regulatory loop between PTEN and PI3K/AKT in renal fibrosis induced by miR-214, but this conclusion needs further experimental confirmation.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Hou

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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The microRNA-214 (miR-214) precursor is formed by the DNM3 gene on human chromosome 1q24.3, which is encoded and transcribed in the nucleus and processed into mature miR-214 in the cytoplasm. Association of miR-214 with the interstitial fibrosis of the kidney has been reported in existing research. Renal interstitial fibrosis is considered necessary during the process of various renal injuries in chronic kidney disease (CKD). One of the important mechanisms is the TGF- (transforming growth factor-) β1-stimulated epithelial interstitial transformation (EMT). The specific mechanisms of miR-214-3p in renal interstitial fibrosis and whether it participates in EMT are worthy of further investigation. In this paper, we first demonstrated modulation of the downstream PI3K/AKT axis by miR-214-3p through targeting phosphatase and tension protein homologues (PTEN), indicating the miRNA’s participation in unilateral ureteral obstruction (UUO) nephropathy and TGF-β1-induced EMT. We overexpressed or silenced miR-214-3p and PTEN for probing into the correlation of miR-214-3p with PTEN and the downstream PI3K/AKT signalling pathways. According to the results of the study, miR-214-3p overexpression silenced PTEN, activated the PI3K/AKT signalling pathway, and exacerbated EMT induced by TGF-β1, while miR-214-3p knockdown had the opposite effect. In miR-214-3p knockdown mice, the expression of PTEN was increased, the PI3K/AKT signalling pathway was inhibited, and fibrosis was alleviated. In conclusion, miR-214-3p regulates the EMT of renal tubular cells induced by TGF-β1 by targeting PTEN and regulating the PI3K/AKT signalling pathway. Furthermore, miR-214-3p knockdown can reduce renal interstitial fibrosis through the PTEN/PI3K/AKT pathway.

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Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer

Shi,

Yao,

Shen

et al. 2024

Heliyon

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RETRACTED ARTICLE: Testis developmental related gene 1 promotes non-small-cell lung cancer through the microRNA-214-5p/Krüppel-like factor 5 axis

Cited by 6 publications

References 48 publications

Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Britannin inhibits cell proliferation, migration and glycolysis by downregulating KLF5 in lung cancer

Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer

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