LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC

Zhuang, Cheng‐Le; Ma, Qian; Zhuang, Changshui; Ye, Jing; Zhang, Fangting; Gui, Yaoting

doi:10.1096/fj.201900078rr

Cited by 71 publications

(58 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Correlation between miR-182-5p expression and clinicopathological characteristics of renal cell cancer patients[3,48,49] (Clear cell renal cell carcinoma)…”

mentioning

confidence: 99%

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

102

View full text Add to dashboard Cite

Background: Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are potential biomarkers that play key roles in tumor development and progression. Urothelial cancer associated 1 (UCA1) is a novel lncRNA that acts as a potential biomarker and is involved in the development of cancers. However, the molecular mechanism of UCA1 in renal cancer is still needed to further explore. Methods: The relative expression level of UCA1 was determined by Real-Time qPCR in a total of 88 patients with urothelial renal cancer and in different renal cancer cell lines. Loss-of-function experiments were performed to investigate the biological roles of UCA1 and miR-182-5p on renal cancer cell proliferation, migration, apoptosis and tumorigenicity. Comprehensive transcriptional analysis, dual-luciferase reporter assay and western blot etc. were performed to explore the molecular mechanisms underlying the functions of UCA1. Results: In this study, we found that UCA1 was significantly up-regulated in renal cancer. Moreover, increased UCA1 expression was positively correlated with differentiation and advanced TNM stage. Further experiments demonstrated that knockdown of UCA1 inhibited malignant phenotypes and Notch signal path of renal cancer cells, and miR-182-5p was reverse function as UCA1. UCA1 functioned as a miRNA sponge to positively regulate the expression of Delta-like ligand 4(DLL4) through sponging miR-182-5p and subsequently promoted malignant phenotypes of renal cancer cells, thus UCA1 playing an oncogenic role and miR-182-5p as an antioncogenic one in renal cancer pathogenesis. Conclusion: UCA1-miR-182-5p-DLL4 axis is involved in proliferation and progression of renal cancer. Thus, this study demonstrated that UCA1 plays a critical regulatory role in renal cancer cell and UCA1 may serve as a potential diagnostic biomarker and therapeutic target of renal cancer.

show abstract

“…Correlation between miR-182-5p expression and clinicopathological characteristics of renal cell cancer patients[3,48,49] (Clear cell renal cell carcinoma)…”

mentioning

confidence: 99%

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

102

View full text Add to dashboard Cite

show abstract

“…Functionally, upregulated lncRNAs generally promote tumorigenesis by promoting cell proliferation, metastasis and inhibiting apoptosis [ 26 , 27 ]. In our study, loss-of function assay proved that silencing of ACTA2-AS1 in CC significantly inhibited cell proliferation, migration, colony-forming capacity and caused G1 phase arrest.…”

Section: Discussionmentioning

confidence: 99%

A novel mechanism by which ACTA2-AS1 promotes cervical cancer progression: acting as a ceRNA of miR-143-3p to regulate SMAD3 expression

Luo

Wang

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Long non-coding RNAs (LncRNAs) have been increasingly confirmed to be abnormally expressed in human cancer and closely related to tumorigenesis. LncRNA ACTA2-AS1 is abnormally expressed in multiple tumors and participates in their development. However, whether ACTA2-AS1 plays a role in the development of cervical cancer (CC) and the exact mechanism of its role has not been elucidated. Methods: Quantitative real-time PCR (qRT-PCR) was conducted to detect the expression level of messenger RNA of ACTA2-AS1, miR-143-3p and SMAD3 in tumor tissues and cells. Additionally, SMAD3 protein expression by western blots in cells. Small interference RNA against ACTA2-AS1 or SMAD3 and miR-143-3p mimic/inhibitor was designed and transfected into CC cell lines to investigate their correlations and potential impacts on cell function. Cell Counting Kit-8 (CCK-8) assay, colony formation, cell cycle assay, transwell assay and flow cytometry analysis were performed to detect the specific effects on cell line proliferation, metastasis and apoptosis. Results: ACTA2-AS1 was significantly increased in CC tissues and cells and miR-143-3p was down-regulated. Clinically, the higher expression of ACTA2-AS1 was significantly correlated with higher FIGO stage. Loss-of-function assay revealed that silencing of ACTA2-AS1 inhibited cell proliferation, colony formation, migration and promoted apoptosis in CC. Additionally, Pearson correlation analysis showed that the expression of ACTA2-AS1 and miR-143-3p were negatively correlated. Dual-luciferase reporter assay and further mechanistic experiments confirmed that ACTA2-AS1 could sponge and regulate the expression of miR-143-3p. Furthermore, SMAD3 was the target gene of miR-143-3p and ACTA2-AS1 could upregulate SMAD3 through acting as a competitive endogenous RNA (ceRNA) of miR-143-3p. Finally, rescue assay demonstrated that the ACTA2-AS1/miR-143-3p/SMAD3 axis played an important role in the proliferation, migration and apoptosis of CC cells. Conclusions: In summary, our study revealed that ACTA2-AS1 upregulates SMAD3 by competitively binding miR-143-3p, thereby accelerating CC progression. The ACTA2-AS1/miR-143-3p/SMAD3 axis can play a crucial role in cervical carcinogenesis, providing new clues for the early diagnosis and treatment of CC.

show abstract

“…circ-HIPK3 is a newly identified circRNA, which can promote the proliferation and invasion of glioma cells via the miR-124-3p/STAT3 axis. 21 Identification of the potential miRNA sponged by circ-HIPK3. (A) Schematic representation of the potential binding sites of miR-338-3p with circ-HIPK3 (https:// circinteractome.nia.nih.gov/) and the mutation sites for specific assay; (B), double luciferase reporter assay in the SiHa and C-4I cells co-tranfected with circ-HIPK3WT or mutated reporter with or without miR-338-3p mimics; (C), miR-338-3p in the CC cell lysates was pulled down and enriched with biotin-labeled miR-338-3p specific probe; (D) the miR-338-3p expression level in the human CC cells (HeLa, CaSki, SiHa, C-33A, C-4I, SW756) and the normal human cervical epithelial End1/E6E7 cells; (E), the miR-338-3p expression levels in paired CC and adjacent normal tissues from 45 CC patients (same samples as in Figure 1A) detected by qRT-PCR; (F) the miR-338-3p expression levels in circ-HIPK3-silenced SiHa and C-4I cells detected by qRT-PCR; (G) Pearson correlation analysis of the association between miR-338-3p with circ-HIPK3 in the CC tissues from the 45 CC patients (same samples as in Figure 1A).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, a novel circRNA, circ-HIPK3 was reported to promote the proliferation and invasiveness of glioma cells through sponging miR-124-3p to up-regulate the STAT3 expression. 21 Abnormal expression of miR-338-3p has been reported to be extremely related with the development and prognosis of multiple cancers. [22][23][24][25][26][27] However, the relationship between circ-HIPK3 and miR-338-3p, also their function and clinical application in CC remain unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>Circular RNA HIPK3 Promotes EMT of Cervical Cancer Through Sponging miR-338-3p to Up-Regulate HIF-1α</p>

Qian

Huang

Wen

2020

CMAR

View full text Add to dashboard Cite

Background: Cervical cancer (CC) is the 4th most common malignancy and cancer-related fatality in women worldwide. Circular RNA is a newly recognized noncoding RNA form. More reports have confirmed their important regulatory functions in diverse physiological and cancer processes. However, the function and mechanisms of circ-HIPK3 in CC remain unknown. Methods: circ-HIPK3 expression status was verified between 45 paired CC and normal adjacent tissues from 45 CC patients, also the 6 CC cell lines and a normal human cervical epithelial End1/E6E7 cell line by qRT-PCR. Effects of circ-HIPK3 silence on CC cell phenotypes were estimated. Circular RNA interactome was applied to forecast binding site between circ-HIPK3 and miRNAs. Pearson correlation analysis was used to confirm the relationship between genes. Point mutation, RNA pull-down, luciferase assay and rescue experiments were applied for molecular mechanism exploration. Results: circ-HIPK3 expression was significantly elevated in CC cells and tissues. circ-HIPK3 silence repressed growth and metastasis, while induced apoptosis in CC cells. circ-HIPK3 sponged miRNA-338-3p (miR-338-3p); miR-338-3p to up-regulate hypoxia-inducible factor-1α (HIF-1α) and CC progress. MiR-338-3p silence or HIF-1α over-expression rescued circ-HIPK3 knockdown caused inhibition of CC malignant characteristics. Conclusion: circ-HIPK3 acts as a competing endogenous RNA of miR-338-3p to promote cell growth and metastasis in CC, via regulating HIF-1α mediated EMT. Therefore, targeting circ-HIPK3/miR-338-3p/HIF-1α axis may be a novel therapeutic strategy for CC.

show abstract

LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC

Cited by 71 publications

References 43 publications

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

A novel mechanism by which ACTA2-AS1 promotes cervical cancer progression: acting as a ceRNA of miR-143-3p to regulate SMAD3 expression

<p>Circular RNA HIPK3 Promotes EMT of Cervical Cancer Through Sponging miR-338-3p to Up-Regulate HIF-1α</p>

Contact Info

Product

Resources

About