Evidence map›Paper›PMID 41299565›Full record

ArticleJournal of translational medicine2025

DCST1-AS1 promotes renal cell carcinoma progression via regulating the miR-582-5p/HMGB2 axis.

Chuanjing Dai, Jiannan Hu, Xiong Tian, Hanxi Zhou, Zhenyu Yang, Shunqiao Jin, Jingmin Zheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

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

7 authors.

Chuanjing DaiDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China.ORCID 0000-0003-0760-1418
Jiannan HuDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China.
Xiong TianDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China.
Hanxi ZhouDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China.
Zhenyu YangDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China.
Shunqiao JinDepartment of Dermatology, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Zhejiang, China.
Jingmin ZhengDepartment of Public Experimental Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, Zhejiang, 317000, China. zhengjingmin@enzemed.com.

Funding

Science and Technology Plan Project of Taizhou 24ywb26
6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) represents between 80 and 90% of primary renal cancers. While long non-coding RNAs (lncRNAs) are documented to modulate RCC development, their biological functions remain poorly understood.

methodsRNA sequencing data from 541 RCC and 71 adjacent normal tissues were downloaded from TCGA database. Kaplan-Meier survival, ROC curve, and clinicopathologic analyses were used to examine the prognostic value of the lncRNA DCST1-AS1 in RCC. The levels of DCST1-AS1 in RCC tissues and cell lines were assessed using quantitative PCR, and its subcellular localization was examined using fluorescence in situ hybridization and RNA nuclear-cytoplasmic separation assays. The functional role of DCST1-AS1 was investigated through a series of in vitro experiments including CCK-8, colony formation, wound-healing, and Transwell assays, as well as in RCC xenograft mice. The targets of DCST1-AS1 were examined using RNA-pull down, luciferase reporter, and RNA immunoprecipitation assays, while Western blotting and immunofluorescence were utilized for investigation of the potential involvement of the PI3K/AKT/GSK-3β axis.

resultsDCST1-AS1 levels were observed to be elevated in both RCC tissues and cell lines, with raised levels linked to advanced tumor stage, pTNM stage, and unfavorable patient prognosis. DCST1-AS1 knockdown reduced proliferation, migration, and cell cycle progression in RCC cells. Conversely, DCST1-AS1 overexpression promoted both tumorigenesis and metastasis in xenograft mice. Mechanistically, DCST1-AS1 enhanced HMGB2 expression by sponging miR-582-5p. Moreover, DCST1-AS1 overexpression stimulated the PI3K/AKT/GSK-3β axis and nucelar translocation of β-catenin. Further functional experiments confirmed that LY294002, a PI3K-specific inhibitor, could attenuate the tumor-promoting effects induced by DCST1-AS1 overexpression.

conclusionsDCST1-AS1 promotes RCC progression by modulation of the miR-582-5p/HMGB2 axis, and may thus have clinical potential in treating RCC.

Indexed as

Carcinoma, Renal CellDisease ProgressionHMGB2 ProteinKidney NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsBase SequenceCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansMaleGlycogen Synthase Kinase 3 betaHMGB2 ProteinMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingDCST1-AS1HMGB2miR-582-5pRenal cell carcinomaTumorigenesis

Identifiers

PMID41299565
PMCPMC12659367

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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 Socratic graph.