DNMT3B regulates proliferation of A549 cells through the microRNA‑152‑3p/NCAM1 pathway

Yang, Bo; Huang, Shiqing; Chen, Hongming; Li, Rizhu; Hou, Shihao; Zhao, Jingjing; Li, Yepeng

doi:10.3892/ol.2021.13129

Cited by 6 publications

(8 citation statements)

References 26 publications

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“…LINC01089 acts as a ceRNA for miR‐152‐3p to repress NSCLC development 24 . Our previous study has demonstrated that miR‐152‐3p inhibits cell proliferation and invasion of A549 cells via regulation of NCAM1 6 . Here, we discovered that miR‐152‐3p inhibited autophagy and suppressed cisplatin chemoresistance in A549/DDP and H446/DDP cells.…”

Section: Discussionmentioning

confidence: 69%

“…24 Our previous study has demonstrated that miR-152-3p inhibits cell proliferation and invasion of A549 cells via regulation of NCAM1. 6 Here, we discovered that miR-152-3p inhibited autophagy and suppressed cisplatin chemoresistance in A549/DDP and H446/DDP cells. Furthermore, autophagy activator rapamycin could overturn the inhibited autophagy and cisplatin chemoresistance induced by miR-152-3p in vitro, indicating that miR-152-3p suppressed drug chemoresistance through inhibition of autophagy.…”

Section: Discussionmentioning

confidence: 84%

“…5 Our previous study has demonstrated that DNMT3B regulates the proliferation of A549 cells through the miR-152-3p/NCAM1 pathway. 6 Importantly, miR-152-3p is implicated in modulating autophagy in acute myeloid leukemia. 7 DNA methyltransferase 1 (DNMT1) represses mitophagy and exacerbates heart failure through miR-152-3p.…”

Section: Introductionmentioning

confidence: 99%

“…Autophagy is a catabolic process that captures and degrades cellular waste in lysosome, 4 which is a physiological mechanism for cell survival effectively applied by cancer cells to cause drug resistance 5 . Our previous study has demonstrated that DNMT3B regulates the proliferation of A549 cells through the miR‐152‐3p/NCAM1 pathway 6 . Importantly, miR‐152‐3p is implicated in modulating autophagy in acute myeloid leukemia 7 .…”

Section: Introductionmentioning

confidence: 99%

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ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

Zhao

Zhang

et al. 2023

Cancer Science

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Resistance to chemotherapeutic drugs limits the efficacy of chemotherapy in non–small cell lung cancer (NSCLC). Autophagy is an essential mechanism which involves in drug resistance. Our previous research has revealed that miR‐152‐3p represses NSCLC progression. However, the mechanism of miR‐152‐3p in autophagy‐mediated chemoresistance in NSCLC remains unclear. Cisplatin‐resistant cell lines (A549/DDP and H446/DDP) were transfected with related vectors and subjected to cisplatin, autophagy inhibitor, activator, or extracellular signal–regulated kinase (ERK) activator. Flow cytometry, CCK8 and colony formation assays were performed for testing apoptosis and cell viability. The related RNAs or proteins were detected by qRT‐PCR or Western blot. Chromatin immunoprecipitation, luciferase reporter assay or RNA immunoprecipitation were used for validating the interaction between miR‐152‐3p and ELF1 or NCAM1. Co‐IP verified the binding between NCAM1 and ERK. The role of miR‐152‐3p in cisplatin resistance of NSCLC was also validated in vivo. The results showed that miR‐152‐3p and ELF1 were decreased in NSCLC tissues. miR‐152‐3p reversed cisplatin resistance by inhibiting autophagy through NCAM1. NCAM1 promoted autophagy through the ERK pathway and facilitated cisplatin resistance. ELF1 positively regulated miR‐152‐3p level by directly interacting with miR‐152‐3p promoter. miR‐152‐3p targeted NCAM1 to regulate NCAM1 level and then affected the binding of NCAM1 to ERK1/2. ELF1 inhibited autophagy and reversed cisplatin resistance through miR‐152‐3p/NCAM1. miR‐152‐3p inhibited autophagy and cisplatin resistance of xenograft tumor in mice. In conclusion, our study revealed that ELF1 inhibited autophagy to attenuate cisplatin resistance through the miR‐152‐3p/NCAM1/ERK pathway in H446/DDP and A549/DDP cells, suggesting a potential novel treatment strategy for NSCLC.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

Zhao

Zhang

et al. 2023

Cancer Science

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“…The knockdown of PRSS23 also affects the molecular interactions. Bo Yang et al found that DNMT3B mediates the proliferation of cancer cells through the NCAM1 pathway 42 . Xiaofang Li et al found that the expression of HIST1H2BD was signi cantly correlated with the survival rate of cervical squamous cell cancer patients 43 .…”

Section: Discussionmentioning

confidence: 99%

PRSS23 (Serine Protease 23) is required for the progression of gastric cancer

Wang¹,

Li²,

He³

2022

Preprint

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PRSS23 (Serine Protease 23) is a vital serine protease that is related to various types of cancers. However, the correlation between PRSS23 and gastric cancer remains unclear. In our study, our objective is to identify the key biomarkers and signaling pathways by analyzing the RNA-seq data. The GSE204725 was created by the Illumina HiSeq 4000 (Homo sapiens). The gene enrichment study indicated the cAMP signaling pathway and Calcium signaling pathway are the main biological processes during the knockdown of PRSS23 in gastric cancer. Moreover, we identified several interactive genes including NCAM1, HIST1H2BD, VWF, HIST1H2BL, GATA1, RYR2, CHRD, PDE4B, HIST1H4B, and HIST2H4B. Our study may provide new knowledge on the treatment of gastric cancer.

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