SPP1 knockdown inhibits invasion, migration and paclitaxel-induced Epithelial-Mesenchymal Transition in Cervical Cancer Cells through the TGF-β/Akt/Snail pathway

Secreted Phosphoprotein 1 (SPP1) was reported to promote the progression of multiple tumors by modulating the immune microenvironment and facilitating metastasis, but its role in cervical cancer remains unclear. Our purpose was to explore the effect and the potential mechanisms of SPP1 on cervical cancer progression and paclitaxel (PTX)-induced epithelial-mesenchymal transition (EMT). The Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) database were used to detect SPP1 expression in human cervical cancer and para-carcinoma non-tumor tissues, immunohistochemistry and western blotting experiments were carried out to confirm the expression of SPP1 in clinical samples. Cancer cell proliferation and metastasis assays were conducted to detect the effects of SPP1 on cancer progress using normal and SPP1-knockdown cervical cancer cells. Transcriptomics data and protein expression assays were utilized to investigate the mechanism underlying the effect of SPP1 on PTX-induced EMT. The mouse metastasis model was used to detect the effect of SPP1 on PTX-induced EMT during cervical cancer metastasis. SPP1 is highly expressed in cervical cancer clinical samples and is associated with low survival rates, SPP1 knockdown inhibits cervical cancer cell migration and invasion but doesn’t affect cell proliferation. Further studies revealed that SPP1 knockdown suppresses tumor cell EMT through the TGF-β/Akt/Snail pathway. Both in vivo and in vitro data confirmed that SPP1 knockdown alleviates PTX-induced EMT. SPP1 knockdown inhibits the invasion, metastasis and PTX-induced EMT of cervical cancer by suppressing TGF-β/Akt/Snail signaling pathway, and SPP1 is a potential therapeutic target for cervical cancer treatment.