Evidence map›Paper›PMID 39692209›Full record

ArticleMolecular genetics & genomic medicine2024

MiR-766-3p Inhibit the Proliferation, Stemness, and Cell Cycle of Pancreatic Cancer Cells Through the MAPK/ERK Signaling Pathway.

Zhipeng Quan, Ziwei Yin, Yuelin Huang, Xuemei Huang, Hao Huang, Qingrong Mo, Jianhua Gong, Lingyun Liu, Yi Zhou, Yaqun Yu

Abstract read
In one paragraph

Article in Molecular genetics & genomic medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Zhipeng QuanDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.ORCID https://orcid.org/0000-0002-1079-5666
Ziwei YinDepartment of Oncology, Third Xiangya Hospital, Central South University, Changsha, China.
Yuelin HuangDepartment of General Surgery, Second Xiangya Hospital, Central South University, Changsha, China.
Xuemei HuangDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Hao HuangHealth Management Center, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Qingrong MoDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Jianhua GongDepartment of Hepatobiliary and Pancreatic Surgery, The First College of Clinical Medical Science (China Three Gorges University), Yichang, China.
Lingyun LiuDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Yi ZhouDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Yaqun YuDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.

Funding

Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair GXLIRMMKL-K202009Guangxi Natural Science Foundation 2017GXNSFAA198039Guangxi Natural Science Foundation 2022GXNSFAA035509Guangxi Provincial Natural Science Foundation 2018GXNSFDA281003Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor(Guangxi Medical University), Ministry of Education/Guangxi Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor GKE-KF202203The National Natural Science Foundation of China 82360552The Self‑Funded Scientific Research Project of Guangxi Zhuang Autonomous Region Health Commission Z20200575The Special Fund of the Central Government Guiding Local Scientific and Technological Development by Guangxi Science and Technology Department GuikeZY21195024Yichang medical and health science and technology project A21-2-017
6 · The paper itself

Abstract

backgroundAs a commonly identified cancer in clinics, pancreatic cancer (PC) has poor prognostic outcomes. This work focused on clarifying the association between MIR-766-3P expression and PC development and progression, as well as the possible role as a biomarker in PC.

methodsMIR-766-3P expression within the human PC cells and samples was measured through miRNA RT-PCR. The gene levels regulated by MIR-766-3P were analyzed through western blot (WB) and qRT-PCR. To analyze whether MIR-766-3P was of certain significance in in vitro and in vivo PC cell proliferation, stemness, and cell cycle progression, the gain/loss-of-function assays were performed. Bioinformatics, RNA sequencing (RNA-seq), and luciferase reporter assay were conducted for exploring regulatory role of MIR-766-3P/MAPK1/MAPK/ERK signal axis in PC.

resultIn comparison with the normal controls, MIR-766-3P expression markedly decreased the tissues and cells of PC. Furthermore, MIR-766-3P could remarkably inhibit the proliferation, stemness, cell cycle progression, and development of PC. The analyses using RNA-seq, and dual-luciferase examination showed that MIR-766-3P could directly target mitogen-activated protein kinase 1 (MAPK1). According to Gene Ontology (GO) as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, MIR-766-3P could affect PC malignant phenotype by MAPK1 and the regulation of the MAPK/ERK-related pathway.

conclusionMIR-766-3P has a certain impact on PC malignant phenotype through combining with MAPK1 while regulating MAPK/ERK-related pathway in vitro and in vivo.

Indexed as

Cell ProliferationMAP Kinase Signaling SystemMicroRNAsNeoplastic Stem CellsPancreatic NeoplasmsAnimalsCell CycleCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase 1MAPK1 protein, humanMicroRNAsMIRN766 microRNA, humanMitogen-Activated Protein Kinase 1MAPK1MAPK/ERKMIR‐766‐3Ppancreatic cancer

Identifiers

PMID39692209
PMCPMC11653159

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.