STAMBPL1 (STAM Binding Protein Like 1)

These findings identify STAMBPL1 as a novel oncogenic DUB that promotes GC progression through IQGAP1 stabilization and subsequent activation of JAK2/STAT3 signaling, providing a potential therapeutic target for GC.

The study underscores the critical role of SMAD3 in modulating Sestrin2 expression and stability, consequently impacting GC cell behaviors and metastatic potential. The SMAD3-Sestrin2 axis emerges as a promising therapeutic target for GC treatment.

Our previous research revealed that the deubiquitinase STAMBPL1 enhances the stability of MKP-1, thereby promoting cisplatin resistance in breast cancer...Furthermore, we discovered that STAMBPL1 regulates GRHL3 transcription by interacting with the transcription factor FOXO1. These findings shed light on the role and mechanism of STAMBPL1 in the pathogenesis of breast cancer, offering novel targets and avenues for the treatment of triple-negative and advanced breast cancer.

This study firstly reveals that STAMBPL1 promotes cholangiocarcinoma progression by upregulating NRF2, indicating that targeting the STAMBPL1/NRF2 axis is a novel therapeutic strategy. Additionally, our findings firstly suggest that LDA can bind to STAMBPL1, inhibiting NRF2 deubiquitination and offering significant therapeutic potential.

Furthermore, STAMBPL1 silencing and the tyrosine kinase inhibitor (TKI) sunitinib also exhibited a synergistic effect on the suppression of KIRC. Collectively, targeting the STAMBPL1/TRIM21/AXL axis can decrease mesenchymal phenotype and potentiate anti-tumor efficacy of cancer therapy.

Inhibition of STAMBPL1 or TOE1 synergistically improves the antitumor activity of lenvatinib. Our work shows the mechanism of STAMBPL1 in liver cancer and suggests it as a potential therapeutic target for liver cancer treatment.

These results underscore the therapeutic potential of CS-6 in HCC treatment. The study offers novel insights into the mechanism of CS-6, suggesting that its therapeutic efficacy may be uniquely mediated by targeting STAMBPL1. This distinct mechanism sets CS-6 apart from existing HCC treatments and positions it as a promising candidate for further clinical investigation.

Modulation of Wnt/β-catenin and lipid metabolism may contribute to its pro-cancer effects. STAMBPL1 may serve as a therapeutic target of HCC.

Cancer treatment reduced most of the serum fusion transcript levels. Serum fusion gene machine learning models may serve as important tools in screening HCC and monitoring the impact of HCC treatment.

The 251-436 sites of STAMBPL1 particularly interact with the 294-496 sites of TRAF2, thereby exerting the function of DUB and removing the ubiquitin molecules attached to TRAF2. Our research unveiled a new function of STAMBPL1 in mediating TRAF2 deubiquitination and stabilization, thereby activating the WNT/PI3K/NF-kb signaling pathway, suggesting its potential as a novel biomarker and therapeutic target for HCC.

Knockdown of STAMBPL1 inhibited cell growth and metastasis of CRC through inactivation of the NF-κB pathway.

The expression of STAMBPL1 mRNA is significantly up-regulated in LUAD, promoting the progression of LUAD by down-regulating the expression of DHRS2 and acting as a potential biomarker of LUAD.