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Recent insight into the role of receptor tyrosine kinase function in cancer cells culminated in the design of highly selective tyrosine kinase inhibitors.
Another important issue that needs to be addressed is clarification of the Ct-OATP1B3 function in cancer cells.
Additionally, we suggest that minisatellite instability might be associated with MUC2 function in cancer cells.
Our data suggests that AM acts as an VEGF-independent angiogenic factor and a reduction in AM's function in cancer cells and the adjacent tumor microenvironment cells results in reduced neoangiogenesis.
Cdr2 is a tumor antigen expressed in a high percentage of breast and ovarian tumors and is the target of a naturally occurring tumor immune response in patients with paraneoplastic cerebellar degeneration, but little is known of its regulation or function in cancer cells.
Concurrently, GLUT4 has been claimed to function in cancer cells.
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As an initial investigation to identify a putative functional role for CCBE1, we, therefore, investigated whether CCBE1 has a function in cancer cell migration.
Here we show that a cell-penetrating peptide, ReACp53, designed to inhibit p53 amyloid formation, rescues p53 function in cancer cell lines and in organoids derived from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous p53 mutations.
Simultaneously, our results advance the possibility that Ct-OATP1B3 might play yet unidentified roles, in addition to transporter function, in cancer cell biology.
Autophagy is known to display a dual contrasting function in cancer cell biology.
The plasma membrane localization would be compatible with our understanding of CXCR4 function in cancer cell migration and homing [1].
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