Abstract

Translationally controlled tumor protein (TCTP) is an evolutionally highly conserved protein which has been implicated as a biomarker for cancer cell reversion although the mechanism is not very clear. This makes it a potential target for cancer therapy. P53 tumor suppressor protein is important in regulating cell growth, it can induce either growth arrest or programmed cell death (apoptosis). TCTP and P53 has been reported that can regulate the protein level of each other.Here we proved that TCTP is a malignancy state keeper in lung cancer and lower level of TCTP protein made cells more sensitive to stressful condition. No obvious difference has been observed from wildtype and the TCTP knockdown lung cancer cells (A549) when located in the normal circumstances. While under the stressful condition, the existence of higher protein level of TCTP can protect cells from apoptosis. TCTP and P53 formed a feedback signal pathway and through it to regulate the downstream Akt signal pathways to make the lung cancer cells keep a higher metabolism level and protect cancer cells from apoptosis induced by outside stress.

Highlights

  • Lung cancer is a leading cause of mortality worldwide, which led to 1,400,000 people dead each year accounting for about 18% of all cancers

  • The result strongly support the conclusion that Translationally controlled tumor protein (TCTP) has an abnormal high distribution in lung cancer and can be taken as a biomarker for diagnosis

  • Overexpressed of TCTP protein has been observed in lung cancer and it has been considered as a critical biomarker for early stage diagnosis [11]

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Summary

Introduction

Lung cancer is a leading cause of mortality worldwide, which led to 1,400,000 people dead each year accounting for about 18% of all cancers. TCTP was taken as an important target for anticancer drug development since its abnormal distribution pattern in many kinds of tumors [2,3,4]. Multiple cancerrelated functions of TCTP have been reported and it is involved in the whole process of cancer such as tumorigenesis, tumor development, metastasis, and invasion etc. According to the previous studies, TCTP is a ‘broad social’ protein It can regulate and be regulated by lots of different factors. It is very likely that to perform one certain function, TCTP may employ a specific group of partner factors which are very different from the groups of factors employed to perform other functions This make it difficult to figure out www.impactjournals.com/oncotarget precisely what mechanisms and which downstream factors TCTP involved in for a certain function and in turn hamper its clinical application. Precise mechanisms and signal pathways of them are still not for sure

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