Esophageal cancer and the sixth leading cause

Esophageal
cancer (EC) is a highly aggressive malignancy with poor prognosis. It is the
eighth most common type of cancer and the sixth leading cause of death from
cancer worldwide. (13/ 14) EC is divided into
two major histological subtypes, esophageal adenocarcinoma (EAC) and esophageal
squamous cell carcinoma (ESCC), which are widely different regarding the
associated etiological factors, affected populations, geographical incidence, and molecular alterations involved in the
genesis and progression of the disease. (2, 6/ 4, High) Nevertheless, ESCC is the predominant histological subtype, responding for approximately 80% of all EC cases. (4, High/ 2, 9/3, 14). The incidence of EC shows
significant regional differences. Notably, the high ESCC incidence areas are
represented by the Asian belt, region ranging from northern Iran to Central
China, eastern and southern Africa, and parts of Southern Europe and America. (High/ 2,3 15/ 1 13). It is reported that alcohol,
tobacco and opium consumption, nutritional de?ciencies, very hot beverages
drinking habits, low socioeconomic status, and genetic predisposition are major risk factors for the
development of ESCC. (4, 13/ 5,6 11/ 4, 6/ 8 High).
Even though diagnostic and treatment methods have been developed in recent years, the overall
five-year survival rate for the ECSS patients remains < 14% .( 1, 11/ 2, 10). Thus, more sensitive and specific biomarkers for early diagnosis and targeted therapy of ECSS are necessary. Members of the high mobility group A (HMGA) family also known as architectural factors have a similar structure including three AT-hook regions that bind to A/T-rich DNA in the minor groove and additional COOH-terminal domain. (8-12 1). These proteins have no transcriptional activity, but through interacting with other transcription factors, they widely regulate many fundamental cellular process including gene expression, cycle-control, cell growth, apoptosis, transformation, differentiation, migration, cellular senescence, and integration. (18-23 HMGA2) Several studies have shown that HMGA2 was over-expressed in many human malignancies such as prostate cancer, gastric carcinoma, ovarian cancer, colorectal cancer, gall bladder cancer, breast carcinoma, pulmonary carcinoma, oral squamous, cell carcinoma, and effects tumor progression and metastasis. (23-29 HMGA2) Moreover, overexpression of HMGA2 in ECSS has been reported in previous studies. (High/ 6/ 7/ 8/ 9) Furthermore, emerging studies reported that suppression of HMAGA2 expression with short interfering RNA (siRNAs) in various cancer cell line increased spontaneous apoptosis and decreased cell proliferation, migration, and viability. (28-32 HMGA2) Taken together, all the mentioned evidence indicated that HMGA2 might be a significant prognostic marker for ECSS. In the present study, we used the specific siRNA to suppress HMGA2 expression in human ECSS TE8 cell line and studied the effect of HMGA2 silencing on the viability, proliferation, and migration of TE8 cells in vitro.