Abstract
LncRNA LINC00657 has oncogenic or anti-carcinoma roles in different cancers, and yet its detailed molecular mechanism in esophageal cancer (EC) remains unclear. In addition, competitive endogenous RNA (ceRNA) regulatory lncRNA–miRNA–mRNA networks are critical for tumorigenesis and progression. Hence, the present study explored the roles of LINC00657 in EC and identified its relevant ceRNA network. We first detected the expression of LINC00657 in EC. Then, we applied starBase and TargetScan websites to find miR-26a-5p binding to LINC00657 and obtain CKS2 as a target of miR-26a-5p. The roles of LINC00657, miR-26a-5p or CKS2 in the proliferation, migration, invasion, and apoptosis of EC cells were respectively assessed by CCK-8, wound healing assay, transwell invasion assay, and flow cytometry. The changes of the MDM2/p53/Bcl2/Bax pathway were measured via Western blot. The results revealed that LINC00657 showed an aberrant high expression in EC cells, which promoted the growth of EC cells. Additionally, LINC00657 functioned as a sponge of miR-26a-5p, and LINC00657 negatively mediated miR-26a-5p to regulate the growth of EC cells. Furthermore, CKS2 was observed as a direct target of miR-26a-5p, and CKS2 controlled the growth of EC cells via the MDM2/p53/Bcl2/Bax pathway. Moreover, there was a positive correlation between LINC00657 and CKS2. LINC00657 knockdown inhibited CKS2 expression to suppress the proliferation, migration, and invasion of EC cells and induced apoptosis via regulating the MDM2/p53/Bcl2/Bax pathway. Collectively, LINC00657/miR-26a-5p/CKS2 ceRNA network could promote the progression of EC, which is good for understanding the molecular mechanism of EC and offers novel biomarkers for EC diagnosis and therapy.
Highlights
Esophageal cancer (EC) is one of the most common cancers and the sixth leading cause of cancer death in the world [1]
LINC00657 was observed to be overexpressed in EC cells (KYSE-150, ECA-109) as compared with normal esophageal epithelial cells (HEEC), which promoted the growth of EC cells
The results showed that LINC00657 functioned as a sponge of miR-26a-5p, and CKS2 was identified to be a target of miR-26a-5p
Summary
Esophageal cancer (EC) is one of the most common cancers and the sixth leading cause of cancer death in the world [1]. Esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) are known as two main histological types of EC [2]. There are approximately 79% of ESCC cases occurring in the Asian countries, while the incidence of EAC has a rapid increase in Western industrialized nations [3]. Risk factors for ESCC mainly include poor nutrition, nicotine consumption, hot beverage drinking, and alcohol abusing [4]. Barrett’s esophagus (BE), advancing age, gastric reflux, male sex, smoking, and obesity are known as EAC’s risk factors [5]. Surgical resection, an invasive and complex treatment, may cause severe postoperative complications, leading to death [5]. In advanced or metastatic EC, License 4.0 (CC BY)
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