Cell Death Differ: TRIM28-RLIM-MDM2-p53 paths affect the development of lung cancer

Lung cancer is one of the leading causes of cancer death worldwide and has now killed more than 1 million people worldwide.
because of the high late-stage diagnosis and metastasis potential of the disease, the five-year survival rate of lung cancer is only 15%.
Anticancer drugs such as gefitinib and erlotinib that target RTK (the subject tyrosine kinase) or EGFR (the skin growth factor complex) have shown some efficacy in patients, but most patients with non-small cell lung cancer (NSCLC) still exhibit resistance and tumor metastasis.
TRIM28 (also known as KAP1 or TIF1-β) is an E3 ubiganic connective enzyme with a variety of in-cell regulation functions, which serves as a co-inhibitor of nuclear positioning and is capable of DNA damage response and maintenance of stem cell potentiality.
previous studies have shown that TRIM28, in collaboration with MDM2, regulates the ubibinization and degradation of p53 in osteosarcoma cells.
TRIM28's characteristics in lung cancer tissue In this study, researchers aimed to identify new lung cancer biomarkers, and by detecting changes in protein expression levels in tumor tissue and corresponding non-tumor tissue in lung cancer patients, researchers found that TRIM28 protein was highly expressed in lung cancer tissue.
further studies have shown that stable over-expression of TRIM28 can significantly improve cell proliferation, migration and invasion in lung cancer cell and transplant tumor models, while knocking down TRIM28 has the opposite effect.
, the researchers revealed that TRIM28 plays a role in cancer-causing genes in lung cancer, which can reduce p53 expression levels by targeting the ubiganic connective enzymes RLIM and MDM2.
and the level of expression of TRIM28 and RLIM was associated with the overall survival rate of the patient.
-related pattern diagram, the above findings illustrate the precise regulatory mechanism of trim28-RLIM-MDM2-p53, which also provides new insights into the development of lung cancer, which may be a potential therapeutic target for the disease.
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