RNF6 (Ring Finger Protein 6)

RNF6 contributed to OC malignancy by destabilizing NME4 and activating the JNK cascade. This newly identified RNF6/NME4/JNK axis provides potential targets for therapeutic intervention in OC.

ABN-B inhibits glioblastoma by inducing cell cycle arrest, senescence, and apoptosis through destabilizing RNF6 and disrupting the RNF6/p27 pathway. Our findings reveal the anti-cancer effect of ABN-B and suggests its potential as a therapeutic candidate or adjuvant for glioblastoma therapy.

our findings define the role of DLG4 that can diminish NSCLC cell proliferation and tumorigenesis through degrading STAT3 in an RNF63-dependent manner. This work suggests a new treatment strategy against NSCLC caused by aberrant activation of STAT3.

On the other hand, RNF6 interacted with SKP2 and stabilized its protein levels in an Akt-dependent manner. Collectively, our data indicated that RNF6 accelerated glioblastoma cell proliferation and tumorigenesis by targeting p27 for degradation.

Therefore, RNF6 is a novel E3 ligase of CCND2 and suppresses LUAD cell proliferation. Implications: This study reveals a novel regulation on cell cycle transition in LUAD and suggests the RNF6/CCND2 axis may represent an alternative therapeutic target for the treatment of LUAD.

Our research reveals that RNF6 is highly expressed in CC, driving malignant progression by upregulating YAP1 protein expression and enhancing the transcription of downstream target genes CTGF and CYR61, offering potential therapeutic targets for CC treatment.

The tankyrase inhibitor XAV939, effectively prevents RNF166-dependent destabilization of angiomotins and subsequent activation of YAP...Importantly, the C-terminus of RNF66, particularly the Di19-ZF domain, is the crucial region responsible for recognizing ADP-ribosylated angiomotins. Together, this work not only sheds light on the regulation of the Hippo pathway in colorectal cancer but also uncovers a novel poly(ADP-ribose)-binding domain, which may serve as a potential therapeutic target for intervention.

Silencing CCNA1/CREBBP partially reversed the promoting effect of RNF6 overexpression on the biological function of GC cells. Our study suggests that RNF6 promotes the progression of GC by regulating CCNA1/CREBBP transcription.

High MKRN1 levels promote TGF-β signalling through ubiquitination and degradation of SNIP1, thereby facilitating CRC metastasis, and supporting MKRN1 as a CRC pro-cancer factor. The MKRN1/SNIP1/TGF-β axis may be a potential therapeutic target in CRC.

In conclusion, TRIM26 is a ubiquitin ligase of PBX1 and it promotes while PBX1 inhibits NSCLC tumor growth. TRIM26 might be a novel therapeutic target for the treatment of NSCLC.

These results indicated that the upregulation of PCGF6 facilitated MAZ/CDK4 axis expression and pRCC progression by hypomethylation of the MAZ promoter. The PCGF6/MAZ/CDK4 regulatory axis may be a potential target for the treatment of ccRCC.