Evidence map›Paper›PMID 38476086›Full record

ArticleCancer science2024

LncRNA CTBP1-AS inhibits TP63-mediated activation of S100A14 during prostate cancer progression.

Guangzheng Wu, Zhenkun Dong, Yuhang Dong, Yinmei Chen, Huan Zhu, Dexin Ding, Yan Cui, Yiwen Wang, Yangyang Xu, Hui Chen

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Guangzheng WuDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Zhenkun DongDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yuhang DongDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yinmei ChenDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Huan ZhuDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Dexin DingDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yan CuiDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yiwen WangDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yangyang XuDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Hui ChenDepartment of Urology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0002-0107-041X
Harbin Medical University · CN

Funding

Haiyan Fund JJZD2022-09
6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) have emerged as important molecules and potential new targets for human cancers. This study investigates the function of lncRNA CTBP1 antisense RNA (CTBP1-AS) in prostate cancer (PCa) and explores the entailed molecular mechanism. Aberrantly expressed genes potentially correlated with PCa progression were probed using integrated bioinformatics analyses. A cohort of 68 patients with PCa was included, and their tumor and para-cancerous tissues were collected. CTBP1-AS was highly expressed in PCa tissues and cells and associated with poor patient prognosis. By contrast, tumor protein p63 (TP63) and S100 calcium binding protein A14 (S100A14) were poorly expressed in the PCa tissues and cells. CTBP1-AS did not affect TP63 expression; however it blocked the TP63-mediated transcriptional activation of S100A14, thereby reducing its expression. CTBP1-AS silencing suppressed proliferation, apoptosis resistance, migration, invasion, and tumorigenicity of PCa cell lines, while its overexpression led to inverse results. The malignant phenotype of cells was further weakened by TP63 overexpression but restored following artificial S100A14 silencing. In conclusion, this study demonstrates that CTBP1-AS plays an oncogenic role in PCa by blocking TP63-mediated transcriptional activation of S100A14. This may provide insight into the management of PCa.

Indexed as

Cell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticProstatic NeoplasmsRNA, Long NoncodingTranscription FactorsTumor Suppressor ProteinsAlcohol OxidoreductasesAnimalsApoptosisCalcium-Binding ProteinsCell Line, TumorCell MovementHumansMaleMiceAlcohol OxidoreductasesCalcium-Binding ProteinsRNA, AntisenseRNA, Long NoncodingS100A14 protein, humanTP63 protein, humanTranscription FactorsTumor Suppressor ProteinsCTBP1‐ASprostate cancerS100A14TP63transcription

Identifiers

PMID38476086
PMCPMC11093200
OpenAlexW4392742286

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 OpenQuestion graph.