LINC00152 facilitates tumorigenesis in esophageal squamous cell carcinoma via miR-153-3p/FYN axis

[Display omitted] •LINC00152 expression is increased in ESCC tumor tissues and cells.•LINC00152 knockdown represses ESCC progression in vitro and in vivo.•LINC00152 functions as a ceRNA to negatively regulate miR-153-3p in ESCC cells.•miR-153-3p-mediated tumor suppressive effect is partly reversed by LINC00152 in ESCC.•FYN, a downstream target of LINC00152/miR-153-3p, facilitates proliferation and lowers apoptosis in ESCC cells. Long non-coding RNAs (LncRNAs) have been found to be associated with the biological behaviors of human cancers. LINC00152 is reported as an oncogene in many kinds of malignancies. However, the functions and mechanisms of LINC00152 involved in esophageal squamous cell carcinoma (ESCC) remain elusive. Our results revealed that LINC00152 expression was up-regulated in ESCC, and correlated with advanced TNM stage, lymph node metastasis, and poor prognosis of ESCC patients. Functionally, LINC00152 knockdown suppressed proliferation, decreased colony forming ability, and induced apoptosis in ESCC cells. Mechanically, LINC00152 functioned as a competing endogenous RNA (ceRNA) to sponge miR-153-3p, thereby facilitating its downstream target FYN. Moreover, miR-153-3p-mediated tumor-suppressive effects were partly reversed following LINC00152 overexpression. Also, FYN knockdown displayed a similar anti-cancerous role in ESCC cells. Taken together, LINC00152 contributed to ESCC progression by down-regulating miR-153-3p and promoting FYN expression, uncovering a novel LINC00152/miR-153-3p/FYN regulatory pathway in ESCC.