LncRNA‐TCONS_00026907 is involved in the progression and prognosis of cervical cancer through inhibiting miR‐143‐5p

Jin, Xuejing; Chen, Xiangjian; Hu, Yan; Ying, Furong; Zou, Ruanmin; Lin, Feng; Shi, Zhengzheng; Zhu, Xuejie; Yan, Xiaojian; Shi, Li; Zhu, Hua

doi:10.1002/cam4.1084

Cited by 62 publications

(49 citation statements)

References 45 publications

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“…Cervical cancer is one of the most common malignant tumors, and its incidence is only preceded by breast cancer [ 1 2 ]. In recent years, more attention is paid to study the role of lncRNA in cervical cancer [ 39 40 ]. In our previous study, lncRNA XLOC_006390 was found to exhibit abnormal expression in cervical cancer cells and influence cervical cancer cell proliferation and migration by regulating downstream SET8 proteins [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

2018

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ObjectiveCervical cancer is one of the most common malignant tumors. Our previous results showed that long non-coding RNA (lncRNA) XLOC_006390 plays an important role in cervical cancer. In this study, we have explored the mechanism of action of lncRNA XLOC_006390.MethodsLncRNA XLOC_006390 was proposed to exercise its function as a competing endogenous RNA (ceRNA), and its potential targeted miRNAs was predicted through the database LncBase Predicted v.2. Two miRNAs, miR-331-3p, and miR-338-3p, were chosen for the study. Expression of miRNAs and lncRNA in cervical cancer cells and tissues was detected by reverse transcription polymerase chain reaction. To determine the correlation, silencing of XLOC_006390, over-expression of miR-331-3p, and miR-338-3p was performed in SiHa and Caski cell lines, respectively.ResultsBased on the interactive effect between miRNA and lncRNA, miR-331-3p and miR-338-3p were significantly downregulated in cervical cancer cells and tissues, and their expression levels were negatively related to that of lncRNA. Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006390 was knocked down. Further, XLOC_006390 was found to facilitate cervical cancer tumorigenesis and metastasis by downregulating miR-331-3p and miR-338-3p expression.ConclusionTaken together, our study demonstrated that XLOC_006390 may serve as a ceRNA and reversely regulates the expression of miR-331-3p and miR-338-3p, thus facilitating cervical cancer tumorigenesis and metastasis.

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Section: Discussionmentioning

confidence: 99%

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

2018

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“…LncRNA CASC2 can suppress epithelial‐mesenchymal transition of hepatocellular carcinoma cells via targeting miR‐367 (Wang, Liu et al, ). LncRNA‐TCONS_00026907 is involved in cervical cancer progression through inhibiting miR‐143‐5p (Jin et al, ). LncRNA MALAT1 can promote metastasis and proliferation by acting as a ceRNA of miR‐144‐3p in osteosarcoma cells (Wang, Yang et al, ).…”

Section: Discussionmentioning

confidence: 99%

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Liu

Yuan

Sun

et al. 2018

Journal Cellular Physiology

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Osteosarcoma is recognized as a malignant tumor in the skeletal system. Long non-coding RNAs (lncRNAs) have been exhibited to play crucial roles in osteosarcoma development. Our current study focused on the biological effects and mechanism of LINC00968 in osteosarcoma pathogenesis. We observed that LINC00968 was dramatically elevated in osteosarcoma cells including U2OS, MG63, Saos-2, SW1353, and 143-B cells compared to human osteoblast cell line hFOB. Silence of LINC00968 inhibited osteosarcoma cell growth and proliferation in vitro. Reversely, overexpression of LINC00968 promoted osteosarcoma cell survival and cell colony formation ability in Saos-2 and 143-B cells. In addition, LINC00968 was able to induce osteosarcoma cell migration and invasion through up-regulating MMP-2 and MMP-9 protein levels. The phosphoinosmde-3-kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway has been reported to participate in several cancer types. Here, in our study, we found that PI3K/AKT/mTOR pathway was involved in osteosarcoma progression. Knockdown of LINC00968 inactivated PI3K/AKT/mTOR signaling pathway in vitro. Subsequently, in vivo tumor xenografts were established using 143-B cells to investigate whether LINC00968 can induce osteosarcoma development in vivo. Consistently, it was indicated that inhibition of LINC00968 significantly inhibited osteosarcoma progression in vivo. Taken these together, in our research, LINC00968 could be provided as a novel prognostic biomarker and therapeutic target in osteosarcoma diagnosis and treatment.

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“…Furthermore, the interactions between lncRNAs and miRNAs in human carcinomas are attracting more and more attention these days. LncRNA‐TCONS_00026907 is found to regulate the progression cervical cancer by targeting miR‐143‐5p (Jin et al, ). By inhibiting miR‐874, lncRNA‐XLOC_008466 can promote human non‐small cell lung cancer development (Yang, Ruan, Hu, Cao, & Song, ).…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

Chang

2017

Journal Cellular Physiology

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Oral squamous cell carcinoma (OSCC), as the most common type of oral cancer, is responsible for almost 3% of all malignant tumors worldwide. Non-coding RNAs such as lncRNAs and microRNAs have been involved in many cancers including OSCC. Recently, lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) has been reported to play an oncogenic role in OSCC metastasis. However, the underlying mechanism of MALAT1 in regulating OSCC progression remains unclear. The aim of this study was to investigate the specific role of MALAT1 in OSCC development. It was observed that MALAT1 was upregulated in OSCC cell lines. Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression. In addition, bioinformatics search was used to identify that miR-125b was a direct target of MALAT1, which indicated a negative correlation between MALAT1 and miR-125b. Besides these, STAT3 was predicted as a binding target of miR-125b in OSCC. Overexpression of MALAT1 was able to suppress the tumor inhibitory effect of miR-125b mimics via upregulating STAT3. Moreover, the function of MALAT1 in OSCC development was further investigated by using in vivo assays. The established nude mice models revealed that downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR-125b/STAT3 axis, respectively. In conclusion, MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR-125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment.

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LncRNA‐TCONS_00026907 is involved in the progression and prognosis of cervical cancer through inhibiting miR‐143‐5p

Cited by 62 publications

References 45 publications

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

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