Lnc-CC3 increases metastasis in cervical cancer by increasing Slug expression

Jiang, Bimei; Sun, Ruili; Fang, Sheng; Qin, Chuan; Xi, Peng; Peng, Li; Li, Yuehui; Li, Guancheng

doi:10.18632/oncotarget.9519

Cited by 22 publications

(26 citation statements)

References 48 publications

(42 reference statements)

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“…There are also many types of lncRNAs that have been studied. Growing evidence suggests that lncRNAs are closely related with tumor . For example, lncRNA H19 promotes breast cancer progression, and plasma circulating lncRNA H19 can also serve as a screening and diagnostic marker for early breast cancer .…”

Section: Discussionmentioning

confidence: 99%

“…Growing evidence suggests that lncRNAs are closely related with tumor. [13][14][15][16][17][18] For example, lncRNA H19 promotes breast cancer progression, and plasma circulating lncRNA H19 can also serve as a screening and diagnostic marker for early breast cancer. 19 In endometrial carcinoma, it has been found that the expression profiles of lncRNAs are different between patients at early stage (stage I/II) and advanced stage (stage III/IV).…”

Section: Discussionmentioning

confidence: 99%

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lncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR

Wang

Chen

et al. 2018

Molecular Carcinogenesis

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lncRNA DLEU1 as a non-coding gene, involves in the occurrence and development of multiple tumors. However, there is no related report in endometrial carcinoma. In order to focus on the role and mechanism of lncRNA DLEU1 in endometrial carcinoma, we used qRT-PCR to detect the expression of lncRNA DLEU1 and found that lncRNA DLEU1 was highly expressed in endometrial carcinoma compared to normal endometrium. Moreover, compared to Ishikawa and KLE, lncRNA DLEU1 was higher in HEC-1B. In addition, up-regulation of lncRNA DLEU1 promoted cell viability, migration, invasion, and reduced the proportion of apoptosis. Otherwise, down-regulation of lncRNA DLEU1 produced opposite results. Xenograft nude mice model assay showed that lncRNA DLEU1 can promote tumorigenesis in vivo. RiP confirmed that lncRNA DLEU1 could bind to mTOR. The rescue experiments revealed that silence of mTOR after up-regulation of lncRNA DLEU1 resulted in decrease of cell viability, migration, and invasion and increase of apoptosis. The expression changes of PI3K, AKT1, p70S6K, rpS6, GSK3β, STAT3, and Bcl-xl were consistent with lncRNA DLEU1 and mTOR in Western blot. Thus, we suggest that lncRNA DLEU1 combines with mTOR and then increases the expression of PI3K/AKT/mTOR pathway to promote endometrial carcinoma tumorigenesis and progression. The present discovery has probability to provide a biomarker and lay the foundation for targeted therapy of endometrial carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

lncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR

Wang

Chen

et al. 2018

Molecular Carcinogenesis

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“…In turn, Slug also bound and activated the promoter of H19 to upregulate its expression, thus forming a positive feedback loop between Slug and H19/miR-675 [50]. Besides H19, several other lncRNAs are now reported to play a pivotal role in regulating the expression and activity of Snail factors, such as LINC01013 [127], lnc-GNAT1-1 [128], and Lnc-CC3 [129]. However, our current knowledge of the crosstalk between lncRNAs and Snail factors is still limited and further studies are necessary to understand the precise relationship between them.…”

Section: Snail/slug and Lncrnasmentioning

confidence: 99%

Missing Links in Epithelial-Mesenchymal Transition: Long Non-Coding RNAs Enter the Arena

Wang

Yang

Jia

et al. 2017

Cell Physiol Biochem

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Cancer metastasis occurs through a series of sequential steps, which involves dissemination of tumor cells from a primary site and colonization in distant tissues. To promote the invasion-metastasis cascade, carcinoma cells usually initiate a cell-biological program called epithelial-mesenchymal transition (EMT), which is orchestrated by a set of master regulators, including TGF-β, Snail, ZEB and Twist families. The biological activities of these molecules are tightly regulated by a variety of cell-intrinsic pathways as well as extracellular cues. Recently, accumulating evidence indicates that long non-coding RNAs (lncRNAs) represent some of the most differentially expressed transcripts between primary and metastatic cancers. LncRNAs including MALAT1, HOTAIR, H19, LncRNA-ATB, and LincRNA-ROR have been reported to be involved in the process of EMT, mainly through cross-talking with master regulators of EMT. Thus, understanding the different and precise molecular mechanisms by which functional lncRNAs switch EMT on and off is important for opening up new avenues in lncRNA-directed diagnosis, prognosis, and therapeutic intervention against cancer.

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“…16 Lnc-CC3 increases metastasis in CC. 17 Nonetheless, there are many lncRNAs remaining poorly understood, and unveiling new CC-related lncRNAs may be beneficial to find new treatment strategies for CC. DGUOK-AS1 was an upregulated lncRNA in CESC tissues according to TCGA public database.…”

Section: Discussionmentioning

confidence: 99%

DGUOK‐AS1 promotes cell proliferation in cervical cancer via acting as a ceRNA of miR‐653‐5p

Song

Ren

et al. 2020

Cell Biochemistry & Function

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Cervical cancer (CC) holds the second highest incidence and is the fourth dominating cause of cancer-induced death in women. It has been widely accepted that long noncoding RNAs (lncRNAs) are implicated in pathological and physiological activities of CC. However, the research of lncRNAs is still in the initial stage. The biological function of lncRNA deoxyguanosine kinase antisense RNA 1 (DGUOK-AS1) in human cancers has not been reported yet. We found that DGUOK-AS1 was aberrantly upregulated in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues through TCGA database. Real-time quantitative polymerase chain reaction (RT-qPCR) also verified the high expression of DGUOK-AS1 in CC cell lines. Loss-of-function assays indicated that DGUOK-AS1 silence repressed CC cell growth. In addition, dual-luciferase reporter and RNA immunoprecipitation (RIP) experiments validated the binding relation between miR-653-5p and DGUOK-AS1 or EMSY. Results of the rescue assays elucidated that EMSY overexpression or miR-653-5p downregulation reversed the suppressive function of DGUOK-AS1 knockdown on cell growth and DNA repair in CC. To sum up, this research highlighted that DGUOK-AS1 could promote CC cell proliferation via serving as a ceRNA of miR-653-5p to release EMSY, which might inspire us to discover novel strategies for CC treatment. Significance of the study: DGUOK-AS1 knockdown hinders proliferation of CC cells. DGUOK-AS1 sequesters miR-653-5p to elevate EMSY in CC. EMSY is required for DGUOK-AS1 to induce cell proliferation and repress DNA damage in CC.

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Lnc-CC3 increases metastasis in cervical cancer by increasing Slug expression

Cited by 22 publications

References 48 publications

lncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR

lncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR

Missing Links in Epithelial-Mesenchymal Transition: Long Non-Coding RNAs Enter the Arena

DGUOK‐AS1 promotes cell proliferation in cervical cancer via acting as a ceRNA of miR‐653‐5p

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