scholarly journals Long non-coding RNA SND1-IT1 accelerates cell proliferation, invasion and migration via regulating miR-132-3p/SMAD2 axis in retinoblastoma

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 1189-1201
Author(s):  
Dong-Fang Yin ◽  
Xue-Jun Zhou ◽  
Na Li ◽  
Hui-Jie Liu ◽  
Hu Yuan
2019 ◽  
Vol 9 (6) ◽  
pp. 822-828
Author(s):  
Zhaohua Cheng ◽  
Weidong Jiang ◽  
Yingbo Han ◽  
Ping Duan

Background: Hepatocellular carcinoma has low levels of long non-coding RNA (LncRNA) RP1130. However, the effects of LncRNA RP1130 in hepatocellular carcinoma still unknown. Materials and Methods: Expression of LncRNA RP1130-1 in HCC and cell lines were detected by real-time PCR. Cell proliferation was assessed by CCK-8. Wound-healing and Transwell assays were performed for HCC cell migration and invasion. Western blotting was carried out to evaluate cell cycle, migration and invasion associated proteins in HCC. Results: Expression levels of LncRNA RP1130-1 was dramatically lower in HCC tissues than in normal control. Similarly, LncRNA RP1130-1 was downregulated in HCC cell lines compared with LO2. The cellular experiments revealed that high expression of LncRNA RP1130-1 in HCC inhibited cell proliferation, migration and invasion. In addition, overexpression of LncRNA RP1130-1 inhibited the expression of transforming growth factor (TGF)-β, and TGF-β reversed the effects of LncRNA RP1130 in HCC cell lines. Conclusions: LncRNA RP1130 exerts anti-tumor effects mediated by inhibiting TGF-β. In summarize, our results indicate that LncRNA RP1130/TGFβ may be a potential therapeutic target for HCC.


2020 ◽  
Vol 10 (3) ◽  
pp. 306-314
Author(s):  
Tingyun Cui ◽  
Dechun Gui ◽  
Chao Gu ◽  
Shuai Yan ◽  
Yinzi Yue ◽  
...  

This study aimed to investigate the effect and mechanism of long non-coding RNA FLVCR1-AS1 on proliferation, invasion and migration of colorectal cancer. QRT-PCR was used to detect the expression of FLVCR1-AS1 in colorectal cancer. The target genes of FLVCR1-AS1 were predicted using the StarBase and Luciferase assay. The biological function of miR-493-3p through a series of in vitro experiments. We examined the expression of FLVCR1-AS1 in colorectal cancer cell lines was remarkably increased. Interference with FLVCR1-AS1 inhibits proliferation, invasion and migration of colorectal cancer cell lines. MiR-493-3p is a targeted miRNA of lncRNA FLVCR1-AS1, and overexpression of miR-493-3p inhibits proliferation of colorectal cancer cells, invasion and migration of colorectal cancer cells, and it can be reversed by lncRNA FLVCR1-AS1. LncRNA FLVCR1-AS1 acts as miR-493-3p sponge to modulate cancer cell proliferation, invasion and migration in colorectal cancer.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qingjuan Meng ◽  
Ningning Wang ◽  
Guanglan Duan

Abstract Background X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. Methods RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. Results The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. Conclusion XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.


2017 ◽  
Vol 43 (1) ◽  
pp. 405-418 ◽  
Author(s):  
Yaoyao Xiong ◽  
Long Wang ◽  
Yuan Li ◽  
Minfeng Chen ◽  
Wei He ◽  
...  

Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.


Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769979 ◽  
Author(s):  
Shaojie Bi ◽  
Chunyan Wang ◽  
Yixin Li ◽  
Wei Zhang ◽  
Juan Zhang ◽  
...  

Overexpression of Axl has been noted to correlate with several human cancers. However, the regulatory mechanisms and effects of Axl in human neuroblastoma development remain unclear. Here, we explore the expression of Axl in neurobalstoma and related upstream regulatory mechanisms of invasion and migration. We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1. Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. Furthermore, we found that targeting Axl by inhibitor R428 significantly suppressed the abilities of tumor cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.


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