ArticleMolecular and cellular biochemistry2026
ROCK2 regulates a stress-responsive transcriptional state and calcium signaling in renal cell carcinoma.
Article in Molecular and cellular biochemistry, 2026. 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
6 authors.
Funding
Abstract
Renal cell carcinoma (RCC) exhibits marked intratumoral heterogeneity that contributes to disease progression and therapeutic resistance. Although ROCK2 has been implicated in RCC progression, its role in regulating tumor cell heterogeneity and cell-state plasticity remains poorly understood. Using single-cell RNA sequencing, we identified a ROCK2-associated stress-responsive transcriptional state characterized by inflammatory signaling and enhanced calcium pathway activity. ROCK2 knockdown was associated with a lower representation of this transcriptional state together with proliferative tumor cells, and integration with the TCGA-KIRC cohort supported the presence of this stress-associated transcriptional program in bulk RCC tumors. Mechanistically, ROCK2 depletion reduced intracellular calcium levels, suppressed CALM1 and CREB1 expression, promoted apoptosis, and impaired cell-cycle progression and proliferation. Pharmacological restoration of calcium signaling with Bay K8644, together with CALM1 or CREB1 overexpression, partially rescued these defects, supporting functional interactions among ROCK2, calcium signaling, CALM1, and CREB1. Collectively, our findings identify a ROCK2-associated stress-responsive transcriptional state linked to altered calcium signaling and provide new mechanistic insight into RCC cellular heterogeneity, highlighting the functional relationship between ROCK2 and calcium signaling as a potential therapeutic vulnerability in RCC.
Indexed as
Identifiers
42886446What 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.