High expression of spermatogenesis associated serine rich 2 promotes tumorigenicity in esophageal squamous cell carcinoma cells and is associated with poor patient prognosis

Exp Ther Med. 2021 Jul;22(1):698. doi: 10.3892/etm.2021.10130. Epub 2021 May 2.

Abstract

Spermatogenesis associated serine rich 2 (SPATS2), recognized as a cytoplasmic RNA-binding protein, is implicated in the tumorgenicity of several cancers. However, the potential role of SPATS2 in esophageal squamous cell carcinoma (ESCC) is yet to be elucidated. The present study aimed to explore the functional implication of SPATS2 in ESCC. The ESCC cell lines Eca109 and KYSE-150 were used to conduct loss-of-function experiments. The expression patterns of SPATS2 in patients with ESCC were obtained from Oncomine, The Cancer Genome Atlas and Genotype-Tissue Expression databases. Reverse transcription-quantitative PCR and western blot analysis were applied to determine the expression levels of SPATS2 in ESCC cells. The proliferation of ESCC cells was measured via cell proliferation and colony-formation assays. Subsequently, the migration and invasion capacities of ESCC cells were observed using Transwell assays. Finally, the expression levels of P53, cyclin E, matrix metalloproteinase (MMP)-9 and neuronal-cadherin were determined via western blot analysis. SPATS2 was expressed at higher levels in ESCC tissues compared with the controls, and high expression of SPATS2 was associated with poor prognosis. ESCC cell line proliferation, migration and invasion abilities were suppressed after silencing SPATS2. Moreover, following knockdown of SPATS2, the proteins cyclin E, MMP-9 and N-cadherin were expressed at markedly decreased levels, while P53 expression was increased. In summary, the results of the present study suggest that SPATS2 promotes ESCC development and progression, providing potential insights into future ESCC targeted treatment.

Keywords: esophageal squamous cell carcinoma; invasion; migration; proliferation; spermatogenesis associated serine rich 2.

Grants and funding

Funding: No funding was received.