Suppression of <scp>EIF</scp>4G2 by miR‐379 potentiates the cisplatin chemosensitivity in nonsmall cell lung cancer cells

Hao, Guangjun; Hao, Haijun; Ding, Yanhui; Wen, H. Joseph; Li, Xiaofeng; Wang, Qianru; Zhang, Bingbing

doi:10.1002/1873-3468.12566

Cited by 52 publications

(38 citation statements)

References 26 publications

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“…Deregulation of miRNAs has been demonstrated to contribute to cancer progression . In the current study, we paid attention to miR‐379, which has been observed in non‐small cell lung cancer, cervical cancer, breast cancer, and osteosarcoma . Nevertheless, no report on the biological roles of miR‐379 alterations in laryngeal carcinoma has been characterized.…”

Section: Discussionmentioning

confidence: 99%

“…26 In the current study, we paid attention to miR-379, which has been observed in non-small cell lung cancer, cervical cancer, breast cancer, and osteosarcoma. [16][17][18][19] Nevertheless, no report on the biological roles of miR-379 alterations in laryngeal carcinoma has been characterized. We focused on miR-379 as a candidate anti-oncogene in laryngeal carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing studies demonstrated that miRNA was aberrantly expressed in several tumors such as gastric cancer, bladder cancer, breast cancer, pancreatic cancer, and laryngeal squamous cell carcinoma . MiR‐379, located at chromosome 14q32.31, is differentially expressed in many kinds of cancers, suggesting that miR‐379 may exert key functions in cancer development. Nevertheless, little is reported about the biological functions of miR‐379 in laryngeal carcinoma.…”

Section: Introductionmentioning

confidence: 99%

“…15 MiR-379, located at chromosome 14q32. 31, is differentially expressed in many kinds of cancers, [16][17][18][19] suggesting that miR-379 may exert key functions in cancer development. Nevertheless, little is reported about the biological functions of miR-379 in laryngeal carcinoma.…”

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confidence: 99%

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MicroRNA‐379 inhibits laryngeal carcinoma cell proliferation and invasion through directly targeting TCF‐4

Wei

Zhang

Zhao

et al. 2019

The Kaohsiung J of Med Scie

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The expression pattern, functions, and detailed regulatory mechanisms of miR‐379 in laryngeal carcinoma remain unknown. In the present study, we aimed to uncover novel potential miR‐379 targets and shed light on its roles in laryngeal carcinoma. The expression level of miR‐379 was measured based on the data obtained from the TCGA database and the cell lines. After miR‐379 mimic transfection, cell proliferation, invasion and migration assay, and wound‐healing assay in HEp‐2 cell line were implemented to evaluate the effects of miR‐379 on laryngeal carcinoma in vitro. The target genes for miR‐379 in silico were predicted and validated using luciferase reporter assay. The miR‐379 expression level was reduced in laryngeal carcinoma tissues and cell lines. Moreover, miR‐379 overexpression inhibited the cell proliferation, migration, and invasion of laryngeal carcinoma cells. TCF‐4 was detected as a direct target of miR‐379 in laryngeal carcinoma. Furthermore, restored TCF‐4 expression rescued the inhibitory roles of miR‐379 overexpression on cell proliferation, migration, and invasion.Our study for the first time demonstrated that miR‐379/TCF‐4 might involve in the progression of laryngeal carcinoma, and miR‐379 appears to serve as a novel tumor suppressor in laryngeal carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

MicroRNA‐379 inhibits laryngeal carcinoma cell proliferation and invasion through directly targeting TCF‐4

Wei

Zhang

Zhao

et al. 2019

The Kaohsiung J of Med Scie

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“…Tumor recurrence and metastasis are main causes of death in patients with NSCLC, and chemotherapy drug resistance is one of the key factors leading to recurrence and metastasis of NSCLC [6]. Currently, cisplatin is a major drug used in chemotherapy of NSCLC, and it facilitates cross-linking between heavy metal ions and cell DNA chain through the connection with nuclear protein, ultimately damaging DNA [7,8]. NSCLC cells have high sensitivity to cisplatin at early stages of treatment, but most of the cells become resistant to chemotherapy after several cycles, leading to failure of chemotherapy [9].…”

Section: Introductionmentioning

confidence: 99%

CLDN1 Increases Drug Resistance of Non-Small Cell Lung Cancer by Activating Autophagy via Up-Regulation of ULK1 Phosphorylation

Zhao

Jiang

et al. 2017

Med Sci Monit

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BackgroundThe aim of this study was to investigate the expression of CLDN1 in non-small cell lung cancer (NSCLC) and its mechanism of action in cisplatin resistance.Material/MethodsA total of 55 patients with NSCLC admitted to our hospital between October 2013 and October 2015 were included. NSCLC tissues and tumor-adjacent tissues (≥5 cm from tumor edge) were collected. Among the 55 patients, 37 had adenocarcinoma and 18 had squamous cell carcinoma. Quantitative real-time polymerase chain reaction was used to determine mRNA expression, and protein expression was examined using Western blotting. CCK-8 assay was used to determine cell proliferation and Transwell assay was used to detect migration and invasion of the cells. Confocal microscopy was used to observe autophagosomes.ResultsIncreased CLDN1 expression promoted the development and metastasis of NSCLC. CLDN1 expression in A549/CDDP cells was up-regulated at both transcriptional and translational levels. Reduced CLDN1 expression decreased the drug resistance, proliferation, migration, and invasion abilities of A549/CDDP cells. Decreased CLDN1 expression promoted the apoptosis of A549/CDDP cells. CLDN1 enhanced CDDP drug resistance of A549 cells by activating autophagy. CLDN1 promoted the autophagy of A549 cells by up-regulating the phosphorylation level of ULK1.ConclusionsThe present study demonstrates that expression of CLDN1 in NSCLC is up-regulated and it is correlated with clinicopathological features. CLDN1 activates autophagy through up-regulation of ULK1 phosphorylation and promotes drug resistance of NSCLC cells to CDDP.

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LINC01579 promotes cell proliferation by acting as a ceRNA of miR‐139‐5p to upregulate EIF4G2 expression in glioblastoma

Chai

Xie

2019

Journal Cellular Physiology

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Glioblastoma (GBM), a malignant and lethal tumor, remains a big threat to human health and life. Increasing explorations have confirmed that long noncoding RNAs are involved in the tumorigenesis and development of multiple cancers. Nevertheless, the regulatory mechanism of (long intergenic nonprotein coding RNA 1579 LINC01579) in GBM remains to be investigated. In this study, the expression of LINC01579 was upregulated in GBM cells and LINC01579 knockdown inhibited cell proliferation as well as promoted cell apoptosis. Additionally, LINC01579 acted as a sponge for miR-139-5p in GBM and eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) was found to be a downstream target of miR-139-5p. Furthermore, the positive correlation of LINC01579 and EIF4G2 as well as the converse correlation between miR-139-5p and LINC01579 (or EIF4G2) were revealed by the experiments. Based on rescue assays, EIF4G2 overexpression or miR-139-5p inhibitor partially recovered the function of LINC01579 knockdown on cell proliferation and apoptosis. In summary, the results of this study verified that LINC01579 modulated cell proliferation and cell apoptosis in GBM by competitively binding with miR-139-5p to regulate EIF4G2, which provided a new clue to figure out potential therapy for patients suffered from GBM.

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Suppression of EIF4G2 by miR‐379 potentiates the cisplatin chemosensitivity in nonsmall cell lung cancer cells

Cited by 52 publications

References 26 publications

MicroRNA‐379 inhibits laryngeal carcinoma cell proliferation and invasion through directly targeting TCF‐4

MicroRNA‐379 inhibits laryngeal carcinoma cell proliferation and invasion through directly targeting TCF‐4

CLDN1 Increases Drug Resistance of Non-Small Cell Lung Cancer by Activating Autophagy via Up-Regulation of ULK1 Phosphorylation

LINC01579 promotes cell proliferation by acting as a ceRNA of miR‐139‐5p to upregulate EIF4G2 expression in glioblastoma

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