Long Noncoding RNA MLK7-AS1 Promotes Non-Small-Cell Lung Cancer Migration and Invasion via the miR-375-3p/YWHAZ Axis

Jia, Jingzhou; Sun, Jiwei; Wang, Wenbo; Yong, Hongmei

doi:10.3389/fonc.2021.626036

Cited by 4 publications

(1 citation statement)

References 26 publications

(28 reference statements)

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“…However, only a few studies have reported the underlying mechanism of YWHAZ in NSCLC progression. For example, Jia et al reported that the important regulator MLK7-AS1 in NSCLC promoted cell invasion in vitro and in vivo by upregulating the miR-375-3p/YWHAZ axis [ 27 ]. Zhao et al found that 14-3-3ζ and Hsp27 worked together to promote NSCLC progression by participating in TGF-β-induced tumor development [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-185-5p targets tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta to regulate non-small cell lung cancer progression

Ma,

Bai,

Chen

et al. 2023

J Cardiothorac Surg

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Background Lung cancer (LC) is one of the most frequent cancers worldwide, as well as the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC, which accounts for 85% of occurrences) is the main type of LC. MiRNAs appear to play a role in the occurrence and progression of many malignancies, according to mounting data. The underlying mechanism of miRNAs in regulating NSCLC cell biological activity and progression, on the other hand, is still being investigated. Methods QRT-PCR were used to detect miR-185-5p expression and YWHAZ mRNA in NSCLC. The CCK-8 assay was used to determine the tumor cells’ ability to proliferate. Transwall assay was used to test the migratory and invasive properties of cells. Cell apoptosis was detected using flow cytometry. Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ), E-Cadherin, N-Cadherin and cleaved-caspase3 protein expression were assessed using Western Blot. The bioinformatics analysis software StarBase2.0 predicted miR-185-5p downstream targets. To confirm the target association between miR-185-5p and YWHAZ, a luciferase experiment was used. In addition, an NCl-H1299 xenograft model was created to assess the anti-tumor impact of miR-185-5p in vivo. The expression level of YWHAZ in tumor tissues of small xenograft tumor model was detected by immunohistochemistry assay. Results Decreased miR-185-5p expression levels were observed in NSCLC. In vitro, over-expressed miR-185-5p decreased cell viability, proliferation, invasion/migration, and induced cell apoptosis, while inhibiting tumor growth in vivo. Dual-luciferase gene experiments confirmed that YWHAZ binds to miR-185-5p. Overexpression of YWHAZ partially restored the inhibitory effects of miR-185-5p on cell behaviors. Conclusion MiR-185-5p was down-regulated in NSCLC, and that overexpressed miR-185-5p inhibited malignant behaviors of cells and tumor growth by negatively regulating YWHAZ.

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Section: Discussionmentioning

confidence: 99%