RAB25 (RAB25, Member RAS Oncogene Family)

In conclusion, silencing of RAB25 inhibits HBV-associated hepatocellular carcinoma cell-induced hepatic fibrosis by suppressing the PI3K/AKT signaling. RAB25 has been proven to be an underlying target for clinical treatment of HBV-associated liver fibrosis.

Confocal microscopy revealed a dose-dependent increase in integrin β1 and talin expression, with consistent spatial distribution patterns in response to curcumin. This study reports that curcumin acts as an anticancer agent in colon cancer by modulating integrin β1 expression through a talin-mediated pathway rather than through rab25.

Together, our findings indicate that drug-resistant states in HGSOC pre-exist at diagnosis, leading to positive selection and reduced clonal complexity at relapse. We suggest these findings motivate investigation of evolution-informed adaptive treatment regimens to ablate drug resistance in future HGSOC studies.

Here, we adopt a magnetogenetic approach that allows direct manipulation of Rab25 positioning to show that localization to the cell periphery drives the formation of F-actin protrusions. We demonstrate that endogenous Rab25 vesicles coordinate the positioning of key cargos, including the actin regulator FMNL1 and integrin β1, with the activation of Rho guanosine triphosphatases at the plasma membrane to generate and maintain F-actin-rich filopodium-like protrusions and promote cancer cell invasive migration in the three-dimensional matrix.

In turn, stimulated cancer cells favor CAF invasiveness through a mechanism that remains to be identified. These findings uncover a bidirectional crosstalk between cancer cells and CAFs and highlight the importance of context-specific in vitro models to decipher ECM-mediated tumor dynamics.

Finally, in ovarian cancer patients, high ADAMTS5 expression correlated with poor prognosis. Altogether, these data identify ADAMTS5 as a novel regulator of ovarian cancer cell migration and invasion, suggesting it might represent a previously undescribed therapeutic target to prevent ovarian cancer metastasis.

Our findings suggest that genomic variations leading to imbalanced expression of BT molecules across cancers contribute to increased BT, which is closely linked to an immunosuppressive microenvironment. The involvement of multiple cell types and complex intercellular interactions underscores the importance of evaluating dynamic cellular crosstalk in the tumor microenvironment to better understand BT increases and develop more effective immunotherapeutic strategies.

Together, our findings indicate that drug resistant states in HGSOC pre-exist at diagnosis and lead to dramatic clonal expansions that alter clonal composition at the time of relapse. We suggest that combining tumor single cell sequencing with cfDNA enables clonal tracking in patients and harbors potential for evolution-informed adaptive treatment decisions.

Our previous research demonstrated the role of MALAT-1 (Metastasis-associated lung adenocarcinoma transcript 1) in the formation of Erlotinib-resistant LUAD cells...In conclusion, our study reveals overexpress MALAT-1 cause the drug resistance of EGFR-TKIs in non-small cell lung cancer (NSCLC) through the MALAT-1/miR-125/Rab25 axis. These findings present a potential novel therapeutic target and perspective for the treatment of LUAD.

This signature, named KAOS for Keratin-Adhesion-Oncogenes-Suppressors, was significantly associated with reduced tumor size but increased mortality rates. Integrating molecular assessment of non-malignant mammary tissue into disease management could enhance survival prediction and facilitate personalized patient care.

This study confirms that loss of RAB25 and overexpression of mutant H-RAS can drive HMECs toward a mesenchymal stem-like state. Our findings reveal that RAB25 functions as a tumor suppressor gene, and loss of RAB25 could serve as a novel biomarker of the claudin-low type of TNBC.

Through our analysis and comprehensive examination of relevant literature, we suggest that targeting the suppressors of the identified drug-resistant markers, such as the Melanoma Antigen (MAGE) family, Trefoil Factor (TFF) family, and Ras-Associated Binding 25 (RAB25), while enhancing the expression of inducers of the drug sensitivity markers [e.g., Serum Amyloid A (SAA) family], could potentially reduce drug resistance and enhance the effectiveness of chemotherapy for gastric cancer. We expect that the developed strategy will serve as a useful tool for uncovering cancer-related phenotype-specific gene regulatory networks that provide essential clues for uncovering not only drug resistance mechanisms but also complex biological systems of cancer.