| Summary: | 碩士 === 國立中興大學 === 分子生物學研究所 === 96 === Recently, lung cancer has dominantly increased and ranked up to the first place among Taiwanese women died from cancers. Therefore, understanding the tumorigenesis and metastasis in lung cancer is very important. Previously we have identified ppp2r2c, a gene for regulatory subunit of the PP2A complex, by using microarray and array-CGH in lung cancer cell lines that is with various invasive abilities. In order to clarify the role of PPP2R2C in NSCLC, we stably transfect human CL1-5 lung cancer cells with pEF6/V5-PPP2R2C and found decreased invasive activity in the resulting clones compared to control cells. In addition, compare to control cell, cell that overexpresses PPP2R2C decreased proliferation and colony formation rate in soft agar. To address the celluar function of PPP2R2C, we examined the known biochemical regulators of invasion and proliferation. In immunoprecipitation experiment, endogenous c-SRC co-immunoprecipitate with PPP2R2C-V5. Additionally, overexpression PPP2R2C decreased c-SRC activityand markedly suppressed the activation of Ras-ERK1/2 in highly invasive CL1-5. On the other hand, we have identified the interacting proteins of PPP2R2C through affinity purification-based proteomics to sort out the candidate proteins. The result revealed that eukaryotic translation elongation factor 1 gamma (EEF1G) could interact with PPP2R2C. EEF1G encodes a subunit of the elongation factor-1 complex which’s function is known as enzymatic delivery of aminoacyl tRNAs to the ribosome. This study gives us a new annotation of PPP2R2C in cancer metastasis and invasion mechanism and that PPP2R2C might be a promising therapeutic target for cancer metastasis and cell growth.
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