Evidence map›Paper›PMID 39505344›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024

[High KHSRP expression promotes gastric adenocarcinoma metastasis: the mediating role of the JAK1/STAT3 signaling axis].

H Zhang, Y Liu, X Li, M Wang, L Li, H Wei

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

H ZhangDepartment of Gastroenterology, Henan University, Kaifeng 475001, China.
Y LiuInstitute of Nursing and Health, Henan University, Kaifeng 475001, China.
X LiDepartment of Thoracic Surgery, Huaihe Hospital, Henan University, Kaifeng 475001, China.
M WangInstitute of Nursing and Health, Henan University, Kaifeng 475001, China.
L LiInstitute of Nursing and Health, Henan University, Kaifeng 475001, China.
H WeiDepartment of Thoracic Surgery, Huaihe Hospital, Henan University, Kaifeng 475001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the regulatory effect of KHSRP on progression of gastric adenocarcinoma and the role of the JAK1/STAT3 signaling axis in mediating its effect.

methodsKHSRP mRNA expression level was detected using qRT-PCR in 120 pairs of gastric adenocarcinoma and adjacent tissues, 4 gastric adenocarcinoma cell lines (MKN-28, HGC-27, CRL-5822, and SNU-1) and normal human gastric mucosal GES-1 cells. In HGC-27 cells with KHSRP knockdown and SNU-1 cells with KHSRP overexpression, cell proliferation, migration, invasion and expression levels of JAK/STAT were evaluated using CCK-8 assay, Transwell migration and invasion assays, and Western blotting. In BALB/c-nude mice, HGC-27 cells with KHSRP knockdown and SNU-1 cells overexpressing KHSRP were injected either subcutaneous or via the tail vein to observe subcutaneous xenograft growth and lung metastasis of the tumor cells.

resultsGastric adenocarcinoma tissues and cell lines all showed significantly increased KHSRP expression as compared with the adjacent tissues and GES-1 cells. In HGC-27 cells, KHSRP knockdown significantly inhibited cell proliferation, migration and invasion, while KHSRP overexpression enhanced the malignant behaviors of SNU-1 cells. In nude mice, inoculation of HGC-27 cells with KHSRP knockdown resulted in smaller tumor volume and weight, slower cell proliferation rate and fewer lung metastatic foci, and KHSRP-overexpressing SNU-1 cells produced the opposite results. KHSRP knockdown in HGC-27 cells significantly down-regulated the expression levels of JAK1 and STAT3, which were obviously increased in KHSRP-overexpressing SNU-1 cells.

conclusionHigh expressions of KHSRP promote progression and metastasis of gastric adenocarcinoma possibly by regulating the JAK1/STAT3 signaling axis.

Indexed as

AdenocarcinomaCell MovementCell ProliferationJanus Kinase 1Signal TransductionSTAT3 Transcription FactorStomach NeoplasmsAnimalsCell Line, TumorHumansMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeoplasm MetastasisRNA-Binding ProteinsJAK1 protein, humanJanus Kinase 1RNA-Binding ProteinsSTAT3 protein, humanSTAT3 Transcription FactorJAK1KHSRPmolecular mechanismSTADSTAT3

Identifiers

PMID39505344
PMCPMC11744079

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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.