Retracted: CRNDE promotes cell tongue squamous cell carcinoma cell growth and invasion through suppressing miR‐384

Abstract

Tongue squamous cell carcinoma (TSCC) is the most common type of oral cancer and is an aggressive head and neck malignancy. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in diverse biological cell processes, such as cell development, fate decisions, cell differentiation, cell migration, and invasion. In our study, we showed that long noncoding RNA colorectal neoplasia differentially expressed (CRNDE) expression was upregulated in TSCC cell lines and tissues. Overexpression of CRNDE increased the TSCC cell proliferation, cell cycle, and cell invasion. Moreover, ectopic expression of CRNDE inhibited the miR‐384 expression in the SCC1 cell and increased the Kirsten Ras (KRAS), cell division cycle 42, and insulin receptor substrate 1 expression, which were the direct target genes of miR‐384. We demonstrated that the miR‐384 expression was downregulated in the TSCC samples compared with the paired adjacent nontumor samples. The expression of CRNDE was negatively correlated with the expression of miR‐384 in the TSCC samples. Overexpression of miR‐384 suppressed TSCC cell proliferation, cell cycle, and invasion. Furthermore, we demonstrated that CRNDE promoted TSCC cell proliferation and invasion through inhibiting miR‐384 expression. These results suggested that CRNDE acts as an oncogene in the development of TSCC, which partially occurs through inhibiting miR‐384 expression.

Long non-coding RNA CRNDE promote the progression of tongue squamous cell carcinoma through regulating the PI3K/AKT/mTOR signaling pathway

“…20 Moreover, high CRNDE expression was demonstrated to promote cell proliferation, cell cycle and cell invasion in TSCC cell lines by negatively regulating miR-384. 8 In the present study, we veried that CRNDE was upregulated in TSCC tissues and cell lines, in accordance with previous result. 8 We also conformed that high CRNDE expression was associated with poor prognosis of TSCC patients.…”

“…8 In the present study, we veried that CRNDE was upregulated in TSCC tissues and cell lines, in accordance with previous result. 8 We also conformed that high CRNDE expression was associated with poor prognosis of TSCC patients. Furthermore, we found that CRNDE knockdown repressed the proliferation, colony formation, migration and invasion while enhanced the apoptosis in TSCC cells in vitro, in accordance with former work.…”

“…7 A recent document reported that lncRNA colorectal neoplasia differentially expressed (CRNDE) was upregulated in TSCC and high CRNDE expression accelerated the proliferation, cell cycle and invasion of TSCC cells. 8 However, the molecular mechanism of CRNDE involved in TSCC progression is still unknown.…”

Long noncoding RNA CASC9 promotes LIN7A expression via miR‐758‐3p to facilitate the malignancy of ovarian cancer

“…Amounting reports have shown that lncRNAs could regulate cell proliferation, differentiation, stemness, survival, and epithelial–mesenchymal transition (Q. Xu et al, ; Yong et al, ; Zhu, Wang, Huang, et al, 2016). For instance, Ren et al () showed that lncRNA CRNDE is upregulated in tongue squamous cell carcinoma tissues and enhances tumor cell proliferation and metastasis via inhibiting miR‐384. L. Xu et al () reported that lncRNA LINC01296 overexpression predicts poor prognosis in patients with lung cancer and promotes tumor growth through regulating miR‐598/Twist1 pathway.…”

H3K27ac-induced lncRNA PAXIP1-AS1 exhibits oncogenic property in ovarian cancer by targeting miR-6744-5p/PCBP2 axis

“…Extensive studies have suggested that lncRNAs could modulate survival, cell proliferation, stemness, differentiation, and epithelial-mesenchymal transition (EMT) [8][9][10]. For example, lncRNA CRNDE shows a high level in tongue squamous cell carcinoma tissues and inhibits miR-384 to facilitate cell proliferation and metastasis [11]. Besides, highlyexpressed LINC01296 is revealed to predict poor prognosis in lung cancer patients and enhances tumor growth via modulating miR-598/Twist1 pathway [12].…”