<i>Retracted:</i> Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR‐155‐5p

Tong, Lingling; Yu, Ao; Zhang, Hejia; Wang, Kun; Wang, Yunyun; Ma, Qingjie

doi:10.1002/cam4.2350

Cited by 34 publications

(33 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LncRNAs regulate biological behaviors including cell proliferation, cell apoptosis, cell metastasis etc., during tumorigenesis [11][12][13]. For instance, lncRNA NORAD promoted cell proliferation by competitively binding with miR-155-5p [14]. LINC00339 accelerated cell metastasis in pancreatic cancer by sponging miR-497-5p and modulating IGF1R [15].…”

Section: Introductionmentioning

confidence: 99%

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

2020

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

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

2020

View full text Add to dashboard Cite

show abstract

“…It has been reported that lncRNAs participate in multiple cancers and regulate the chemoresistance of cancer cells, including NSCLC (Nagasaka et al 2018). NORAD has been discovered to be a tumour promoter in several cancers (Tao et al 2019;Tong et al 2019), but little is known whether NORAD can affect the drug resistance of NSCLC cells. In the present study, we investigated the role of NORAD in drug resistance of A549/DDP cells and its potential mechanism.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NORAD/miR-202-5p regulates the drug resistance of A549/DDP to cisplatin by targeting P-gp

Shen¹,

Xu²,

Yin³

2020

gpb

View full text Add to dashboard Cite

In this study, we established the DDP-resistant NSCLC cell line A549/DDP to detect the effect of NORAD on cisplatin resistance of A549/DDP cells. NORAD was highly expressed in A549/DDP cells compared with A549 cells. The MTT data showed that knockdown of NORAD enhanced the inhibition rate of cisplatin on the A549/DDP cells and decreased IC50 value. The colony formation and MTT assay suggested that cisplatin inhibited cell proliferation, and knockdown of NORAD enhanced the inhibitory effect of cisplatin on A549/DDP cells. Besides, we found that NORAD silence reduced the P-gp expression but not BCRP, LRP and MRP. Moreover, NORAD could directly bind to miR-202-5p, and ABCB1 was a target of miR-202-5p. The MTT assay found that miR-202-5p inhibitor reversed the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Then, the Western blot data showed that knockdown of NORAD reduced P-gp expression, and miR-202-5p inhibitor enhanced P-gp expression. ABCB1 overexpression reversed the inhibitory effect of NORAD knockdown on A549/DDP cells. Moreover, NORAD could directly bind to miR-202-5p, and ABCB1 was a target of miR-202-5p. Inhibition of miR-202-5p and overexpression of ABCB1 eliminated the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Overexpression of miR-202-5p suppressed P-gp expression in A549/DDP cells. Collectively, our data showed that NORAD could enhance the DDP resistance of A549/DDP cells and potentially increased P-gp expression by sponging the miR-202-5p.

show abstract

“…Recently, the involvement of miRNAs in tumorigenesis and their signi cance as effective biomarkers are also becoming increasingly appreciated [14]. miR-155-5p has been found to regulate the development of various cancer types, including human epithelial ovarian cancer [16], cervical cancer [17,18], and colon cancer [19]. It has been reported that some certain long non-coding RNAs (lncRNAs) suppress HCC development by sponging miR-155-5p [20]; miR-155-5p modulated the malignancy of HCC by regulating Wnt/β-catenin signaling or suppressing PTEN through the PI3K/Akt pathway [21,22]; therefore, miR-155-5p can be a promising therapeutic target for HCC patients.…”

Section: Discussionmentioning

confidence: 99%

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

Wang

Che

2020

Preprint

View full text Add to dashboard Cite

Background: Hepatocellular carcinoma (HCC) is the leading cause of tumor-related death worldwide due to high morbidity and mortality, yet still lacking biomarkers and therapies. Circular RNAs (circRNAs) are a group of non-coding RNAs that regulate gene expression through interacting with miRNAs, implicating in the tumorigenesis and progression. A novel circRNA, circTP63, was reported to be an oncogene in HCC. However, its role in HCC remains unclear.Methods: qRT-PCR was used to assess the mRNA levels of CircTP63 in 90 pairs of tumor and adjacent normal tissues from HCC patients, one human normal hepatic epithelial cell line and HCC cell lines. CCK-8, colony formation, transwell, and flow cytometry assays were performed to detect the cellular function of circTP63/miR-155-5p/ZBTB18 in HCC cells. Bioinformatic analysis, RNA pull-down and luciferase assays were used to determine the interaction among circTP63/miR-155-5p/ZBTB18. Results: circTP63 was significantly upregulated in HCC tissues and cell lines. High circTP63 expression is closely associated with the tumor stages, lymph node metastasis, and poor prognosis of HCC patients. Functionally, knockdown of circTP63 inhibited cell proliferation, migration, invasion, and promoted cell apoptosis of HCC. Meanwhile, overexpression of circTP63 enhanced HCC progression. Mechanically, circTP63 was a sponge of miR-155-5p to facilitate the ZBTB18 expression, and the ZBTB18 expression in HCC tissues was negatively associated with the survival rate of HCC patients. Furthermore, the reduced tumor-promoting effect on HCC cells induced by knockdown of circTP63 can be reversed by miR-155-5p inhibitor or ZBTB18 overexpression. Conclusion: Our data highlight a critical circTP63-miR-155-5p-ZBTB18 regulatory network involved in the HCC progression, gaining mechanistic insights into the function of CircRNAs in HCC progression, and providing effective biomarkers and therapeutic targets for HCC treatment.

show abstract

Retracted: Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR‐155‐5p

Cited by 34 publications

References 31 publications

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

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

LncRNA NORAD/miR-202-5p regulates the drug resistance of A549/DDP to cisplatin by targeting P-gp

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

Contact Info

Product

Resources

About