PCNA (Proliferating cell nuclear antigen)

Our results suggest that targeting polyamine metabolism with SAM486A enhances the efficacy of KRASG12C inhibitors and may mitigate resistance. This combination represents a promising therapeutic approach for KRASG12C-mutant NSCLC and warrants further clinical investigation.

In vivo, RHART significantly suppressed tumor growth and expression of CPSF6, MCT4, PCNA, and PKM2, while enhancing cleaved caspase-3. These findings provide scientific evidence that RHART induces apoptotic and metabolic reprogramming effects in hepatocellular carcinoma by targeting the CPSF6/MCT4/c-Myc signaling axis, underscoring its potential as a novel natural therapeutic candidate for liver cancer.

Importantly, TRPV1 expression correlated positively with cancer stem cell markers in both murine models and human samples. Collectively, our results reveal that TRPV1 is not only overexpressed in PCa but also contributes to proliferation regulation and stemness features, positioning it as a potential diagnostic and prognostic biomarker for prostate cancer.

While single cases of similar composite neoplasms have been reported in humans, this is the first documented case in a laboratory mouse. These findings expand the known spectrum of spontaneous hematopoietic tumours in aged mice and highlight the importance of comprehensive histopathological and immunophenotypic evaluation in diagnosing atypical lesions.

Across a CRC panel that included SNU-C5/WT and its 5-fluorouracil- and oxaliplatin-resistant derivatives, HT-29 (KRAS-wild-type), and HCT-8 and LoVo (KRAS-mutant), co-immunoprecipitation showed that PrPC forms complexes with the 37/67 kDa laminin receptor (RPSA), with PrPC-RPSA association particularly increased in KRAS-mutant HCT-8 and LoVo cells. Taken together, these findings suggest that extracellular PrPC supports RAS-AKT signaling, proliferation, and tumor-associated angiogenesis in KRAS-mutant colorectal cancer, and that PrPC neutralization additively enhances 5-fluorouracil activity in KRAS-mutant models. The data provide a preclinical basis for evaluating PrPC antibodies in combination with fluoropyrimidine-based regimens in patients with KRAS-mutant CRC.

This study showed that TAS2R14 knockout in oral cancer cells significantly decreased calcium mobilization, increased cell numbers, colony formation, the proliferation marker proliferating cell nuclear antigen, and the phosphorylation of mechanistic target of rapamycin, but did not affect cell viability...Therefore, T2R14 downregulation increased oral cancer CPG, suggesting a tumor-suppressor-like role. The study's findings could improve our understanding of T2R14 mechanisms and help develop strategies to advance oral cancer treatment by targeting T2R14.

Docetaxel (DTX) remains the first-line chemotherapeutic for advanced prostate cancer, however, its therapeutic efficacy remains limited by poor aqueous solubility, rapid systemic clearance, and severe dose-dependent toxicity...Collectively, this "stable-in-circulation, trigger-in-tumor" platform substantially improves intratumoral DTX delivery and apoptosis-driven antitumor efficacy, while maintaining systemic safety. These findings highlight PEG-HMS-DTX as a promising and generalizable strategy for prostate cancer chemotherapy, warranting further pharmacokinetic, immunogenicity, and GLP toxicology studies to support translational advancement.

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.

The anti-hyperproliferation and the anti-inflammatory effects of DHM were attributed to the attenuation of the expression of PCNA, procaspase-3, iNOS, TLR-4, and IL-1β in both the prostate and seminal vesicle tissues. DHM has potential protective effects against testosterone-induced BPH model via downregulation of inflammatory mediators, restoration of oxidative balance, and induction of cell apoptosis.

These findings suggest that WMW intervention is associated with coordinated alterations in inflammation-related signaling, cell proliferation, and extracellular matrix remodeling in CRC, with focal adhesion-YAP-related mechanotransduction representing a potential associated feature. This study provides integrated experimental evidence supporting further investigation of WMW and traditional Chinese medicine-based strategies targeting focal adhesion-associated signaling in CRC research.

These findings related to MYOF-specific effects, as compared to MYON, emphasize that these differences are statistically significant and relevant to UF risk. It can shed insight on how phthalates exposures may impact UF pathogenesis and provide a basis for exploring targeted therapeutic strategies.

Thus, ASE may mitigate liver injury by re-balancing apoptosis-survival signaling and promoting structural recovery. Our interpretation emphasizes that dose, route, and formulation are critical for translational potential.