CHN1 (Chimerin 1)

To summarize, this study gives insights into the functional role of ARHGAP29 and its downstream signaling in melanoma. Our findings provided evidence supporting the hypothesis that ARHGAP29 is an important player in melanoma progression, a promising and novel target in melanoma treatment.

Overall, this study elucidates the crucial role of COL1A1, COL1A2, CHN1, and FN1 in GC pathogenesis and underscores their potential as diagnostic markers and therapeutic targets.

While FAM72's presence as a gene pair with the SLIT-ROBO Rho GTPase-activating protein 2 (SRGAP2) is intriguing, its functional roles, particularly in neural stem cells, remain incompletely understood. This review explores the distinct characteristics of FAM72, shedding light on its expression patterns, potential roles in cell cycle regulation, stem cell renewal and implications in neurogenesis and tumorigenesis.

Expression of ARHGAP29 correlates with the clinical tumor parameters of BC patients. In addition, ARHGAP29 is involved in increased invasiveness of tamoxifen-resistant BC cells. ARHGAP29 alone or in combination with its downstream partners RhoC and pAKT1 could be suitable prognostic markers for BC progression.

Chromatin immunoprecipitation assay confirmed the interaction between PCA3 promoter region and ARHGAP21. This is the first study that described the role of ARHGAP21 in regulating the PCA3 gene under the androgenic pathway, standing out as a new mechanism of gene regulatory control during prostatic oncogenesis.

P=N/A, N=178, Completed, Centre of Postgraduate Medical Education | Recruiting --> Completed | N=50 --> 178 | Trial completion date: Nov 2024 --> May 2024

AAV9-mediated overexpression of Arhgap24 exacerbates intimal hyperplasia. We demonstrate that decreased ARHGAP24 expression restrained VSMC proliferation and dedifferentiation possibly by inactivating both AKT and ERK1/2 signaling pathways, which may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia including restenosis and atherosclerosis.

ARHGAP23 expression was related to clinical prognosis, DNA methylation and immune infiltration. These findings support the potential of ARHGAP23 as a prognostic biomarker and a molecular target for cancer treatment.

P=N/A, N=50, Recruiting, Centre of Postgraduate Medical Education | Trial primary completion date: Nov 2023 --> Feb 2024

ARHGAP21 downregulation can significantly promote the migration and metastatic ability of NSCLC possibly as a result of WNT signaling pathway activation, which reduces the ubiquitination of β-catenin by affecting the expressions of APC, GSK3β, and Axin.

TBX18 knockdown lowered CHN1 transcription and thus reduced RhoA activity, which sensitized ESCC cells to radiotherapy.

In addition, RNA-seq analyses identified four chimeric transcripts (ATG4B::PTMA, OAZ1::PTMA, ZFP36::PTMA, and PIM3::BRD1), two of which (ATG4B::PTMA and ZFP36::PTMA) failed to be detected at the remission, suggesting a possible transcriptional remodeling during the disease course. Overall, our results indicate a favorable prognostic impact of the described chromosomal aberration, as it arises a permissive molecular landscape to the spontaneous B-CLL regression in the patient, highlighting ARHGAP24 as a potentially relevant concurrent alteration to the 13q14 deletion in delineating B-CLL disease evolution.