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Abstract
The objective of this study was to explore the role of the SULF2-mediated ERK/AKT signaling pathway in cervical cancer. SULF2 expression was detected in tumor tissues and tumor-adjacent normal tissues from cervical cancer patients. HeLa cells were divided into six groups: control group, NC group, SULF2 siRNA group, SULF2 group, SULF2 + LY294002 group, and SULF2 + U0125 group. In each group, HeLa cells received the corresponding treatment, followed by measurement of the cellular biological characteristics and expression of the ERK/AKT signaling pathway. We also confirmed the effect of SULF2 in vivo using a xenograft model in nude mice. SULF2 was upregulated in cervical cancer tissues, which was specifically associated with the clinical stage, histological differentiation, and lymphatic metastasis. Compared to the control group, the SULF2 siRNA group displayed decreased expression of SULF2, concomitant with reduced proliferation, migration, and invasion, but there was an increase in the apoptosis rate of HeLa cells, as well as downregulation of the p-Akt/Akt, p-ERK/ERK, and Bax/Bcl-2 ratios and cyclin D1. Additionally, tumor growth was significantly inhibited in the xenograft model of nude mice. The results in the SULF2 group were quite the opposite in which SULF2 facilitated the growth of cervical cancer cells, which was reversed by LY294002 or U0126. SULF2 is highly expressed in cervical cancer, and thus, downregulation of SULF2 can inhibit the ERK1/2 and AKT signaling pathways to suppress the proliferation, invasion, and migration of cervical cancer cells while facilitating apoptosis.
Highlights
Cervical cancer is currently the second leading cause of cancer-related death in females worldwide, second to breast cancer [1]
Statistical analysis revealed that sulfatase 2 (SULF2) expression was correlated with the clinical stage (P= 0.005), histological differentiation (Po0.001), and lymphatic metastasis (P=0.001)
SULF2, the extracellular sulfatase that changes the sulfation of heparan sulfate proteoglycans, was significantly upregulated in cervical cancer, and its higher expression was significantly associated with the clinical stage, histological differentiation, and lymphatic metastasis of cervical cancer, which was consistent with other studies
Summary
Cervical cancer is currently the second leading cause of cancer-related death in females worldwide, second to breast cancer [1]. Evidence has confirmed the involvement of the ERK1/2 signaling transduction pathway in the development of cervical cancer [16,17]. AKT, known as protein kinase B, is a downstream target protein of PI3K and, as the core element of the PI3K/AKT signaling pathway, is crucial in the evolution of tumors, including promoting cell proliferation, Role of SULF2 in cervical cancer anti-apoptosis, and pro-angiogenesis via initiating the downstream substrate [18,19,20]. There remains little information regarding the association between SULF2 and cervical cancer, and we postulated that SULF2 may exert its effect in the development of cervical cancer by regulating the ERK/AKT signaling pathway
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