Abstract
Thymic stromal lymphopoietin (TSLP), produced by cervical cancer (CC) cells, promotes angiogenesis, and the recruitment and functional regulation of eosinophils. It has been reported that microRNA (miR)-132 is aberrantly decreased in CC tissues. However, the function and mechanism of TSLP on the biological behaviors of CC cells is largely unknown. The aim of the present study was to investigate the effect of TSLP on the expression of miR-132 and the proliferation and invasion in vitro of CC cell lines, namely, HeLa and SiHa cells. The transcrpitional level of miR-132 was analyzed using reverse transcription-quantitative polymerase chaon reaction. The proliferation, invasion, and the expression of proliferation and invasion-related molecules in HeLa and SiHa cells in vitro were evaluated using bromodeoxyuridine cell proliferation, Matrigel invasion assays, flow cytometry and ELISA, respectively. Here, it was revealed that recombinant human TSLP (rhTSLP) downregulated the expression levels of miR-132 in HeLa and SiHa cells, and by contrast, the neutralizing antibodies for TSLP or TSLP receptor (TSLPR) upregulated miR-132 expression levels in HeLa and SiHa cells. The overexpression of miR-132 resulted in a lowered proliferation and invasiveness, decreased levels of proliferation-associated molecules marker of proliferation Ki-67 and proliferating cell nuclear antigen, and the decreased production of matrix metalloproteinase (MMP)2 and MMP9 in HeLa and SiHa cells. Compared with the control group, there was a higher level of proliferation and invasion in HeLa and SiHa cells following stimulation with rhTSLP. However, these effects induced by rhTSLP were significantly impaired in HeLa and SiHa cells with miR-132 overexpression. The results of the present study indicated that TSLP produced by CC cells downregulated miR-132 expression, and stimulated the proliferation and invasion of CC cells, thereby further promoting the development of CC.
Highlights
Cervical cancer (CC) is one of the most common gynecological malignancies with high rates of morbidity (0.001‐0.05%) and mortality (0.0024‐0.0175%), endangering the health and quality of life of women globally [1]
In order to evaluate the effect of Thymic stromal lymphopoietin (TSLP) on the expression of miR‐132 in CC cells, HeLa and SiHa cells were treated with with recombinant human TSLP (rhTSLP), α‐TSLP or α‐TSLP receptor (TSLPR). rhTSLP was revealed to downregulate the expression of miR‐132 in HeLa and SiHa cells, with a signficant difference observed at concentrations of 10 and 100 ng/ml (P
An accumulating body of evidence has indicated that miRNAs serve vital functions in the progression of CC and that they directly contribute to the growth and metastasis of CC cells via the targeting of a large number of critical protein‐coding genes. miR‐132 is located on human chromosome 17p13.3, which is associated with various types of human cancer including osteosarcoma, gastric cancer [21], colorectal cancer [22], prostate cancer [23], breast cancer [24,25], hepatocellular carcinoma [26], pancreatic cancer [27,28] and glioma [29]
Summary
Cervical cancer (CC) is one of the most common gynecological malignancies with high rates of morbidity (0.001‐0.05%) and mortality (0.0024‐0.0175%), endangering the health and quality of life of women globally [1]. The pathogenesis of CC remains enigmatic and may be connected with numerous factors, including infection with high‐risk human papillomaviruses (HPVs) [2]. Thymic stromal lymphopoietin (TSLP) is primarily produced by stromal cells, epithelial cells, fibroblasts, keratinocytes, basophils and other types of cells, including mast cells, smooth muscle cells, fibroblasts, dendritic cells, trophoblasts, and cancer or cancer‐associated cells [3,4,5]. A previous study reported that an aberrantly high level of TSLP present in cancer lesions, potentially mediated by hypoxia, was a notable regulator of the progression of CC by recruiting and licensing tumor‐associated eosinophils (EOS) to CC lesions [9]. Watanabe et al [12] reported that high
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