MiR-185-3p mimic promotes the chemosensitivity of CRC cells via AQP5

Zhou, Chunhua; Kong, Wencheng; Ju, Tong-Fa; Xie, Qi; Zhai, Limin

doi:10.1080/15384047.2020.1761238

Cited by 19 publications

(12 citation statements)

References 48 publications

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“…MiRNA plays a momentous role in the progression of CRC by up-regulating oncogenes or down-regulating oncogenes [33]. For example, the latest research found that miR-185-3p is down-regulated in CRC, and upregulating miR-185-3p can enhance the chemotherapy sensitivity of CRC cells by targeting AQP5 [34]. Ma et al found that knocking down LINC02163 attenuated CRC cell proliferation and metastasis through the miR-511-3p/AKT3 axis [35].…”

Section: Discussionmentioning

confidence: 99%

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

Tang

et al. 2021

J. Microbiol. Biotechnol.

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The literature indicates that LINC00174 promotes the growth of colorectal cancer (CRC) cells, but its research needs to be enriched. We tried to explore the function and mechanism of LINC00174 in CRC cell proliferation and migration. Bioinformatics analysis predicted the binding relationship and expressions of lncRNA, miRNA and mRNA. Clinical study analyzes the relationship between LINC00174 and clinical data characteristics of CRC patients. The expressions of LINC00174, miR-3127-5p and E2F7 were verified by RT-qPCR, and the combination of the two was verified by dual luciferase analysis and RNA immunoprecipitation as needed. Western blot was used to detect the expression of EMT-related protein and E2F7 protein. Functional experiments were used to evaluate the function of the target gene on CRC cells. LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients. High-expression of LINC00174, contrary to the effect of siLINC00174, promoted cell viability, proliferation, migration and invasion, up-regulated the expressions of N-Cadherin, Vimentin, E2F7, and inhibited the expression of E-Cadherin. MiR-3127-5p was one of the targeted miRNAs of LINC00174 and was down-regulated in CRC samples. In addition, miR-3127-5p mimic partially reversed the malignant phenotype of CRC cells induced by LINC00174. Besides, E2F7 was a target gene of miR-3127-5p, and LINC00174 repressed miR-3127-5p to regulate E2F7. Our research reveals that LINC00174 affected the biological characteristics of CRC cells through regulated miR-3127-5p/ E2F7 axis.

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Section: Discussionmentioning

confidence: 99%

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

Tang

et al. 2021

J. Microbiol. Biotechnol.

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“…MiR-185-3p, also upregulated in the mutation group, is proven a tumor suppressor in colorectal cancer (CRC) 34 , the overexpression of which could enhance the chemosensitivity of CRC patients. Therefore, it is considered a potential target for the treatment of 5-FU-insensitive CRC 35 .…”

Section: Discussionmentioning

confidence: 99%

Genetic and tumor microenvironment differences between cell cycle progression pathway altered/non-altered patients with lung adenocarcinoma

Shan¹,

Bi²,

Bian³

et al. 2021

Preprint

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Background Lung cancer is the leading cause of cancer-related death worldwide, among which lung adenocarcinoma (LUAD) is the most common type. Identified as a hallmark of cancer, the dysregulated cell cycle progression plays an important role in the promotion and progression of LUAD. This article aims to elucidate the heterogeneity between CDKN2A-CDK/cyclin-RB1 cell cycle progression pathway altered /non-altered patients with LUAD, thus helping us have a better understanding of the effect of the aberrant cell cycle. Material and Methods The data of this study were downloaded from The Cancer Genome Atlas (TCGA) data portal (https://portal.gdc.cancer.gov/) and UCSC Xena Browser (http://xena.ucsc.edu/), including simple nucleotide variation data, RNA-seq gene expression data, survival data, clinical data, and miRNA expression data. After matching the RNA-seq gene expression data, simple nucleotide variation data, miRNA expression data, and survival data with clinical data, 510 gene and long non-coding RNA expression data, 506 simple nucleotide variation data, 440 microRNA expression data, and 497 survival data were included in this study for further analysis. R software (version 4.0.3) was used for analysis. Results After dividing the patients into mutation (n = 57) and wild (n = 453) groups according to the cell cycle progression pathway status, we found no significant difference in survivorship between them. The mutation group had a higher mutational load and mutational rates of various genes such as tumor protein P53 (TP53) compared to the wild group. Subsequently, we analyzed the differentially expressed genes (DEGs) between the two groups. Among the 58387 genes analyzed, 302 were upregulated, and 354 were downregulated in the mutation group. Enrichment analysis indicated that these DEGs were closely related to metabolism items and cell cycle-related events. After performing immune cell infiltration analysis, we found the two groups have different patterns of immune cell profiling. Albeit the immune and stromal scores were higher in the wild group, we failed to find any significant difference between the two groups. Finally, we build a computational model to predict the cell cycle progression pathway-related gene mutation by LASSO-binary logistic regression analysis, the predictive accuracy of which is 0.88. Conclusion In summary, our study compared the genetic and microenvironment differences between cell cycle progression pathway altered /non-altered patients with LUAD by analyzing the data from TCGA datasets. We hope our findings could improve our understanding of the heterogeneity between the two kinds of patients, thus providing new insight into LUAD patients' treatments.

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“…The primers are listed in Table 1 . U6 ( Zhou C. et al, 2020 ) and β-actin ( Li L. et al, 2018 ) act as endogenous controls. Samples were analyzed with the comparative CT method, where fold change was calculated from the ΔΔCT value with the formula 2 –ΔΔ Ct .…”

Section: Methodsmentioning

confidence: 99%

“…By repressing the level of neurofibromatosis 1, the upregulated expression of miR-641 promotes resistance to ER in non-small-cell lung cancer cells (Chen et al, 2018). Previous studies indicated that miR-185-3p can promote the antitumor effect of other antitumor drugs (Uhr et al, 2019;Zhou C. et al, 2020). However, it is not clear whether miR-185-3p affects the ER resistance in lung cancer.…”

Section: Introductionmentioning

confidence: 99%

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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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MiR-185-3p mimic promotes the chemosensitivity of CRC cells via AQP5

Cited by 19 publications

References 48 publications

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

Genetic and tumor microenvironment differences between cell cycle progression pathway altered/non-altered patients with lung adenocarcinoma

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

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