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FAM64A promoted aggressiveness and chemoresistance in colorectal cancer cells by lipogenesis or Akt pathway

ABSTRACT: This dataset was generated based on the hypothesis that FAM64A promotes colorectal cancer aggressiveness by reprogramming the cellular proteome. Quantitative proteomic analysis was performed by LC-MS/MS on three groups of SW480 cells: the FAM64A overexpression group, the FAM64A knockdown group, and the control group. The data showed that FAM64A not only significantly changed the abundance of proteins associated with cell proliferation and invasion but also drove the reprogramming of proteins related to lipid and carbohydrate metabolism. Therefore, these findings provide a molecular mechanism to explain how FAM64A promotes cancer progression. This data is of great value as it can be used to further mine biomarkers, study tumor metabolism, or construct signaling networks.

ORGANISM(S): Homo Sapiens

SUBMITTER: Huachuan Zheng

PROVIDER: PXD068756 | iProX | Wed Sep 24 00:00:00 BST 2025

REPOSITORIES: iProX

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Project description:In this study the investigators looked at adaptive reprogramming impact on the kinome when a MEK inhibitor called GSK1120212 (trametinib) was administered in a "window of opportunity" trial. GSK1120212 is not yet approved by the FDA for use in breast cancer patients. The investigators gave GSK1120212 for a short period of time (one week) to examine MEK and the other kinase expression in cancer cells both before and after the study drug is given. The investigators gave this drug for research purposes only. The length of time it was given is not intended to treat cancer. Recently researchers at UNC developed a process that can comprehensively profile the majority of the individual kinases in the kinome and examine the impact on kinase expression of kinase inhibitors (Duncan et al, Cell 2012, PMID: 22500798). This can tell us which kinases need to be concurrently blocked to augment responsiveness and prevent acquired resistance so that the investigators can design the best combinations of kinase blocking drugs for triple negative breast cancer. This is especially important for individuals with triple negative breast cancer (TNBC) because there are no targeted drugs available that can block molecules that affect tumor growth. The investigators believe that kinase-blocking drugs have the potential to be a more effective treatment for people with TNBC. In this recently published study (Zawistowski et al, Cancer Discovery 2017, PMID: 28108460), TNBC patients treated with trametinib for 7 days resulted in a transcriptional response characterized by significant reprogramming of the tyrosine kinome, and this adaptive bypass response in human tumors was found to be similar to that seen in preclinical models including TNBC cell lines and mouse xenografts. In this study we also examined whether reprogramming differed between TNBC molecular subtypes, finding that basal-like and claudin-low human TNBC cells and mouse tumor subtypes had different adaptive transcriptional responses to MEK-ERK inhibition. Mechanistically we found that genome-wide enhancer remodeling drove the adaptive transcriptional response, suggesting that epigenetic approaches to reprogramming may be more durable than kinase inhibitor polypharmacology.

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FAM64A promoted aggressiveness and chemoresistance in colorectal cancer cells by lipogenesis or Akt pathway

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