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Order Piccovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Salazar-González et al. (2019) used the elaborated E. coli expression system to engineer a putative vaccine candidate against breast cancer. Thus, the two chimeric B19V VP2 were engineered by addition of the epitopes from the insulin-like growth factor-1 receptor (IGF-1R), namely epitopes 249 (GDLTNRCTMEEKPMEK) and P8 (RQPQDGYLYRHNYCSK), to the VP2 N-terminus. This resulted in the multiepitope anticancer VLP vaccine, which prevented and delayed tumor growth when used in a prophylactic scheme of four weekly immunizations prior to cancer cell inoculation in mice and led to idea of a library of chimeric VP2-fused epitopes for further assembly in a designed and personalized epitope delivery system (Salazar-González et al. 2019). To realize this idea, a set of neoepitopes, namely Tmtc2, Gprc5a, and Qars, were selected from experimental studies of next-generation sequencing of the breast cancer 4T1 cell line—as well as an epitope of surviving—and were added to the VP2 N-terminus, and the obtained VLPs were evaluated in a breast cancer model (Jiménez-Chávez et al. 2019).
GPRC5a suppresses the proliferation of non-small cell lung cancer under wild type p53 background
Published in Experimental Lung Research, 2020
Jin Er, Li Chao, Li Yiwei, Xing Feng, Zhao Fei, Wu Kan, Xie Ruifei
GPRC5a, also named retinoic acid-inducible 3 (RAI3), is a family member of the G-protein-coupled receptors, which is the largest protein super family with more than 700 genes in the human genome.19 GPRC5a was originally identified in 1998 in a human oral squamous carcinoma cell line.In the disease context, GPRC5a was originallyreported as a tumor suppressor in non-small cell lung carcinoma. Later its tumor suppressor ability was alsoshown in oral squamous cell carcinoma. Shockingly, subsequent reports indicated that GPRC5a could also behave as an oncogene in breast cancer, colorectal cancer and pancreatic cancer. This dual behavior makes GPRC5a avery interesting target to study. In our previous study, GPRC5a was reported as a tumor suppressor in non-small cell lung cancer (NSCLC).The transcription factor P53mediated the expression of GPRC5a, thus regulated the cell viability as well as apoptosis in NSCLC cells.p53 has been described as the guardian of the human genome, as it conserves genome stability and integrity.20 p53 is a criticalrole for tumor suppress, which acting as a sequence-specific transcription factor, regulates genes by either trans-activation or trans-repression. It was reported that the promoter region of GPRC5a also contains p53DNA binding sequences.3 Over expression of wild-type p53 represses the expression of GPRC5a in ovarian tumor cell line. Both microarray and quantitative RT-PCR showed that GPRC5a mRNA is up-regulatedin breast cancer cell lines which p53 was mutant.3