PRNP (Prion Protein)

In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.

NIST triggered more aggressive tumorigenesis than the synthetic mixture, underscoring the role of particle composition. PM2.5 has environmental and public health impacts, particularly in older adults, and PrPC is a mechanistic regulator and potential biomarker of pollution-associated lung cancer.

These findings revealed an ATIC-associated metabolic-immunoregulatory network in UTUC, through which ATIC supports mTOR-related signaling and promotes tumor progression and cisplatin resistance. Targeting the ATIC-driven network may offer new therapeutic opportunities for UTUC management.

P1, N=30, Not yet recruiting, Broad Institute of MIT and Harvard

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.

It thus can serve as an indicator of tumor invasion, metastasis and prognosis. The knockout of PrPc inhibits growth and migration of tumor stem cells, revealing that PrPc may have the ability to promote the invasion and metastasis of colorectal cancer.

This study provides an overview of cancer-related EV research and identifies key directions for further mechanistic exploration and clinical translation of EVs in precision oncology.

This study demonstrates that PRNP is a key regulator of gemcitabine resistance in PDAC, modulating EMT, ferroptosis, and the tumor immune microenvironment. Targeting PRNP represents a promising therapeutic strategy to reverse gemcitabine resistance and may hold significant potential for clinical translation in PDAC treatment.

Collectively, our findings indicate that while PrPC facilitates early events in αS aggregate interaction with neurons, the sustained neurotoxicity induced by αS prefibrillar oligomers and fibrils is predominantly mediated by extracellular Ca2+. This promotes aggregate-membrane interactions, membrane permeabilization, and intracellular Ca2+ dyshomeostasis, thereby establishing a vicious cycle of neuronal dysfunction and death.

P=N/A, N=150, Recruiting, Massachusetts General Hospital | N=80 --> 150

FOXM1 and PRNP were experimentally evidenced to be highly expressed in meningioma cells, and their knockdown hindered cell growth and migration and triggered ROS accumulation. In summary, our findings established a novel oxidative stress-based molecular classification and identified potential treatment vulnerabilities in high-grade meningiomas, which might assist personalized clinical management.

P=N/A, N=80, Recruiting, Massachusetts General Hospital | Trial completion date: Jun 2025 --> Jun 2027 | Trial primary completion date: Jun 2025 --> Jun 2027