MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

Li, Ké; Yuan, CongHu

doi:10.3892/ijmm.2020.4649

Cited by 20 publications

(15 citation statements)

References 68 publications

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“…[32][33][34][35] miR-103 acts as an oncogene in NSCLC by targeting lncRNA TRHD-AS1, KLF4, and KLF7. 32,36 In DDP-resistant NSCLC cells, the expression of miR-103a-3p is upregulated. 37 miR-103a-3p activates ERK signaling pathway and leads to DDP resistance in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Identification of a competing endogenous RNA axis “SVIL‐AS1/miR‐103a/ICE1” associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis

2021

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Section: Discussionmentioning

confidence: 99%

Identification of a competing endogenous RNA axis “SVIL‐AS1/miR‐103a/ICE1” associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis

2021

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“…MiR-222-3p stimulates the proliferation and represses apoptosis of non-small-cell lung cancer cells via repressing p53 upregulated modulator of apoptosis (PUMA) ( Chen and Li, 2020 ). A study conducted by Li and Yuan (2020) revealed that miR-103 was elevated in A549 and H1299 cells and promoted cell growth and EMT and reduced cell apoptosis. On the contrary, miR-330 represses the viability, proliferation, and migration of lung cancer cells ( Mohammadi et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers

Zhu

Yuan

2021

Front. Cell Dev. Biol.

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Erlotinib (ER), as an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has a significant therapeutic effect in lung cancers. However, EGFR TKI resistance inevitably occurs after treatment for approximately 12 months, which weakens its antitumor effect. Here, we identified miR-185-3p as a significantly downregulated microRNA responsible for acquired EGFR TKI resistance in cells and patients with lung cancer. qRT-PCR and Western Blot were performed to determine the relative expression of miR-185-3p in ER-resistant tumor tissues and cells. The viability and apoptosis of lung cancer cells were evaluated by Cell Counting Kit-8 (CCK8) assay and flow cytometry, respectively. The binding between miR-185-3p and liver-type phosphofructokinase (PFKL) was verified by dual luciferase assay. It was found that overexpression of miR-185-3p conferred ER sensitivity in lung cancer cell lines. MiR-185-3p was downregulated in ER-resistant lung cancer cells (H1299/ER and A549/ER). MiR-185-3p inhibited proliferation and induced cell apoptosis in ER-resistant cells. Mechanistically, miR-185-3p downregulation contributed to ER resistance through upregulating the PFKL. Moreover, Mesenchymal to epithelial transition (MET) oncoprotein promoted EGFR-TKI resistance by regulating miR-185-3p and PFKL. These findings revealed a novel mechanism in which downregulation of miR-185-3p may induce overexpression of PFKL and MET and confer ER resistance in lung cells. Combination of PFKL/MET inhibitors and EGFR TKIs could be a rational therapeutic approach for lung cancer patients with EGFR mutation.

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“…In addition, Li et al have found that regulating KLF7 can inhibit NSCLC invasion, migration, and EMT (28).…”

Section: Discussionmentioning

confidence: 99%

Effects of miR-132-3p on progress and epithelial mesenchymal transition of non-small cell lung cancer via regulating KLF7

Wang¹,

Xu²,

Guo³

et al. 2021

J Thorac Dis

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Background: MicroRNAs (miRNAs) often appear as oncogenes or tumor suppressor genes. The aim of this research was to examine miR-132-3p and Kruppel-like factor 7 (KLF7) effects in the development of non-small cell lung cancer (NSCLC). Methods: We used quantitative reverse transcription polymerase chain reaction (qRT-PCR) to determine miR-132-3p expression in tissue specimens and 6 cells (A549, H1650, H292, H1299, H1944, BEAS-2b).Luciferase report forecasted the targeting relationship between miR-132-3p and KLF7. The expression of KLF7 and interstitial protein was determined by western blot. Proliferation test and Transwell assay were adopted for examining cell development. The Cell Counting Kit-8 (CCK-8) colorimetric method was used to observe the effects of miR-132-3p and KLF7 on the proliferation, metastasis, and invasion of NSCLC tumor cells. In order to determine whether the metastasis of NSCLC tumor cells was epithelialmesenchymal transition (EMT)-mediated, supplementary experiments with E-cadherin and vimentin were performed.Results: An increased expression of miR-132-3p was detected in NSCLC. Its mimic promoted the proliferation of tumor cells. As an immediate site of miR-132-3p, KLF7 was reversely adjusted via miR-132-3p and restrained the development of tumor cells in NSCLC, the effects of which were attenuated via KLF7 over-expression. Besides, the presence of EMT-related diversions was confirmed in NSCLC.Conclusions: By targeting KLF7, miR-132-3p was capable of promoting the proceeding of NSCLC tumor cells. We discovered miR-132-3p/KLF7 route may exhibit curative target for NSCLC.

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MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

Cited by 20 publications

References 68 publications

Identification of a competing endogenous RNA axis “SVIL‐AS1/miR‐103a/ICE1” associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis

Identification of a competing endogenous RNA axis “SVIL‐AS1/miR‐103a/ICE1” associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis

Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers

Effects of miR-132-3p on progress and epithelial mesenchymal transition of non-small cell lung cancer via regulating KLF7

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