LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

Abstract

Liver cancer is now one of the most lethal and commonest cancers in the world, among which over 90% is hepatocellular carcinoma (HCC). Recent studies have confirmed long non-coding RNAs (lncRNAs) are implicated in carcinogenesis. It has been reported lncRNA LINC00668 serves as an oncogene in several cancers. However, the mechanism where LINC00668 regulates HCC is still unclear. qRT-PCR analysis was adopted to detect the expression of relative RNAs. Cytoplasmic and nuclear RNA fraction analysis was conducted to verify the underlying molecular mechanism. Cell colony formation was carried out to test cell colony formation ability and transwell assays were performed to testify cell migratory and invaded abilities. Relevant protein expression level was measured by Western blot assay. LINC00668 was significantly up-regulated in HCC tissues and cell lines. LINC00668 knockdown inhibited cell proliferative, migratory and invasion abilities and slowed down the epithelial–mesenchymal transition (EMT) process. Mechanistically, LINC00668 positively modulates the expression of YY1 by competitively binding to miR-532-5p. It was revealed that LINC00668 up-regulation accelerated cell proliferation and motility in HCC and suggested LINC00668 could be a potential therapeutic target for HCC.

CircANTXR1 Contributes to the Malignant Progression of Hepatocellular Carcinoma by Promoting Proliferation and Metastasis

“…26 In HCC, many researches verified that miR-532-5p was underexpressed in HCC, and it could restrain HCC proliferation, migration and invasion to inhibit cancer development. [27][28][29][30] Similar to these results, our study also revealed that miR-532-5p might play a tumor suppressor role in HCC by inhibiting HCC cell proliferation and metastasis. The reversal effect of anti-miR-532-5p on si-circANTXR1-mediated HCC progression showed that circANTXR1 regulated HCC progression via sponging miR-532-5p.…”

circSKIL promotes osteoblastic differentiation of periodontal ligament cells by sponging miR‐532‐5p to activate Notch signaling

“…27,28 These studies revealed various signaling molecules regulated by miR-532-5p, such as CCR4, RUNX3, RERG, Twist1, YY1, KRAS, and NAP1L1. 22,[24][25][26][27][28] In osteoblasts, parathyroid hormone, an essential regulator for bone remodeling, down-regulated miR-532-5p and released its suppression on matrix metalloproteinase 13. 12 Guo et al reported that miR-532-5p up-regulated in osteoporotic tissues and inhibited osteoblastic differentiation by targeting FOXO1.…”

“…Downstream from circSKIL, we identified miR‐532‐5p as a target sponged by circSKIL and also a negative regulator of Notch1. By far, most studies report miR‐532‐5p as a tumor suppressor in the context of cancer 22–26 and occasionally as an oncogene 27,28 . These studies revealed various signaling molecules regulated by miR‐532‐5p, such as CCR4, RUNX3, RERG, Twist1, YY1, KRAS, and NAP1L1 22,24–28 .…”

“…By far, most studies report miR‐532‐5p as a tumor suppressor in the context of cancer 22–26 and occasionally as an oncogene 27,28 . These studies revealed various signaling molecules regulated by miR‐532‐5p, such as CCR4, RUNX3, RERG, Twist1, YY1, KRAS, and NAP1L1 22,24–28 . In osteoblasts, parathyroid hormone, an essential regulator for bone remodeling, down‐regulated miR‐532‐5p and released its suppression on matrix metalloproteinase 13 12 .…”

Long noncoding RNA small nucleolar RNA host gene 15 deteriorates liver cancer via microRNA‐18b‐5p/LIM‐only 4 axis

“…Accumulating studies have revealed the involvements of long noncoding RNAs (lncRNAs) in oncogenesis and development of liver cancer, such as gastric cancer associated transcript 3 and LINC00668. 5,6 As a component of lncRNAs, small nucleolar RNA host gene 15 (SNHG15) has been developed as an independent role in predicting prognosis of HCC patients, owing to its excessive expression in disease. 7 Abnormal expression of SNHG15 is indicated to connect with advanced clinicopathological traits and poor prognosis in human cancers.…”