Abstract
Thyroid cancer-1 (TC-1), a natively disordered protein, is widely expressed in vertebrates and overexpressed in many kinds of tumors. However, its exact role and regulation mechanism in human non-small cell lung cancer (NSCLC) are still unclear. In the present study, we found that TC-1 is highly expressed in NSCLC and that its aberrant expression is strongly associated with NSCLC cell proliferation. Exogenous TC-1 overexpression promotes cell proliferation, accelerates the cell G1-to-S-phase transition, and reduces apoptosis in NSCLC. The knockdown of TC-1, however, inhibits NSCLC cell proliferation, cycle transition, and apoptosis resistance. Furthermore, we also demonstrated that PD173074, which functions as an inhibitor of the TC-1 in NSCLC, decreases the expression of TC-1 and inhibits TC-1 overexpression mediated cell proliferation in vitro and in vivo. Nevertheless, the inhibition function of PD173074 on NSCLC cell proliferation was eliminated in cells with TC-1 knockdown. These results suggest that PD173074 plays a significant role in TC-1 overexpression mediated NSCLC cell proliferation and may be a potential intervention target for the prevention of cell proliferation in NSCLC.
Highlights
Lung cancer is one of the leading causes of morbidity worldwide
A growing body of evidence shows that Thyroid cancer-1 (TC-1) is an oncogene that is overexpressed in several types of neoplasm [2,3,4,7,8,9,10,11]
The immunohistochemical results showed that TC-1 expression was evident in 90 (73.77%) of the non-small cell lung cancer (NSCLC) tissues and in 18 (14.75%) of the normal lung tissues
Summary
Lung cancer is one of the leading causes of morbidity worldwide. In 2013, approximately 228,190 new cases are projected to occur in the United States, accounting for 13.74% of all new cancer cases. TC-1 was originally cloned from the subtractive hybridization between a papillary thyroid carcinoma and its surrounding normal thyroid tissue [2]. It is expressed ubiquitously across a wide range of vertebrates with the highest conservation across species focused on the open reading frame (ORF). Margaret Sunde et al confirmed that TC-1 is a novel tumorigenic protein associated with thyroid cancer and found that the overexpression of TC-1 in normal thyroid cells increased their proliferation rate, enhanced their anchorageindependent growth in soft agar, and decreased their apoptosis rate [3]. The expression level and the biological function of TC-1 in NSCLC have not heretofore been elucidated
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