ArticleDiscover oncology2025
Roles of KHDRBS2 and KHDRBS3 in prostate cancer progression and AR-V7 regulation.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the biological functions of KHDRBS2 and KHDRBS3 in prostate cancer (PCa) progression and their potential roles in regulating androgen receptor splice variant 7 (AR-V7) expression, a key factor in castration-resistant prostate cancer (CRPC).
methodsWe performed a comprehensive analysis of publicly available datasets to examine the expression patterns of KHDRBS family members in PCa, including CRPC and neuroendocrine subtypes. In vitro experiments were conducted using AR-positive 22RV1 and AR-negative PC3 cell lines to assess the expression and regulatory interactions of KHDRBS2 and KHDRBS3. Functional assays evaluated their effects on cell proliferation and tumor growth in vivo. Additionally, KHDRBS2 protein levels were manipulated in 22RV1 cells to assess their impact on AR-V7 and full-length AR expression.
resultsOur dataset analysis revealed distinct expression patterns of KHDRBS2 and KHDRBS3, with higher alteration frequencies in CRPC and neuroendocrine PCa. In vitro, KHDRBS2 and KHDRBS3 exhibited mutually exclusive expression, with KHDRBS2 predominantly found in AR-positive 22RV1 cells and KHDRBS3 in AR-negative PC3 cells. Reciprocal regulation between the two proteins was observed in both cell lines. Functional studies showed that both KHDRBS2 and KHDRBS3 promoted cell proliferation and tumor growth. Notably, silencing KHDRBS2 in 22RV1 cells led to a selective reduction in AR-V7 expression, without affecting full-length AR levels.
conclusionsThese findings uncover novel roles for KHDRBS2 and KHDRBS3 in PCa progression, with KHDRBS2 identified as a potential key regulator of AR-V7 expression. Our results provide new insights into AR splice variant regulation and highlight potential therapeutic targets for PCa treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.