Long noncoding RNA UCA1 enhances sensitivity to oncolytic vaccinia virus by sponging miR-18a/miR-182 and modulating the Cdc42/filopodia axis in colorectal cancer

Horita, Kosuke; Kurosaki, Hajime; Nakatake, Motomu; Ito, Mai; Kono, Hiromichi; Nakamura, Takafumi

doi:10.1016/j.bbrc.2019.06.125

Cited by 20 publications

(13 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…13,14 In recent studies, UCA1 was reported to promote the progression of paclitaxel resistance in ovarian cancer by regulating the miR-654-5p/SIK2 axis, 15 also enhancing sensitivity to oncolytic vaccinia virus by sponging miR-18a/miR-182 and modulating the Cdc42/filopodia axis in colorectal cancer. 16 Similar findings have also been reported in bladder cancer, 17 breast cancer, 18 ovarian cancer, 19 and lung cancer, 20 namely UCA1 enhanced chemoresistance in cancer. 21 However, the effect of UCA1 on chemoresistance in GC is still unclear.…”

Section: Introductionsupporting

confidence: 68%

LncRNA UCA1 Enhances Cisplatin Resistance by Regulating CYP1B1-mediated Apoptosis via miR-513a-3p in Human Gastric Cancer

Huang

Sharen

Wang

et al. 2021

CMAR

View full text Add to dashboard Cite

Background: Chemoresistance contributes to treatment failure of gastric cancer (GC) patients but the molecular mechanism of chemoresistance in GC is still unclear. Longchain noncoding RNA (lncRNA) urothelial cancer associated 1 (UCA1) is associated with resistance to chemotherapy drugs. Methods: We detected the expression of UCA1 in 53 pairs of GC tumor tissue and adjacent normal tissue, human normal gastric mucosa cells (GES-1) and human GC cells (HGC-27, SNU-5, AGS, SGC-7901, and NCI-N87) using RT-qPCR. Small RNA interference technology was used to knock down the expression of UCA1 in gastric cancer cells. CCK8 solution was used to detect cell viability. Flow cytometry was used to detect apoptosis, and Western blotting was used to detect protein expression. Results: UCA1 was highly expressed in GC tissues and cells, and knockdown of UCA1 increased chemosensitivity to cisplatin by inducing cell apoptosis. Furthermore, UCA1 promoted CYP1B1 expression by binding to miR-513a-3p in human GC cells in vitro, and UCA1/CYP1B1 expression was negatively related to miR-513a-3p expression, while UCA1 expression was positively related to CYP1B1 expression in human GC tissues. Moreover, overexpression of miR-513a-3p or knockdown of CYP1B1 increased chemosensitivity to cisplatin, and knockdown of miR-513a-3p or overexpression of CYP1B1 decreased chemosensitivity to cisplatin by inducing cell apoptosis in human GC cells. Importantly, overexpression of CYP1B1 reduced chemosensitivity to cisplatin which increased by knockdown of UCA1, and knockdown of CYP1B1 increased chemosensitivity to cisplatin which decreased by knockdown of miR-513a-3p in human GC cells. Conclusion: The lncRNA UCA1/miR-513a-3p/CYP1B1 axis regulates cisplatin resistance in human GC cells; hence, it is a potential target for treating chemoresistance in GC.

show abstract

Section: Introductionsupporting

confidence: 68%

LncRNA UCA1 Enhances Cisplatin Resistance by Regulating CYP1B1-mediated Apoptosis via miR-513a-3p in Human Gastric Cancer

Huang

Sharen

Wang

et al. 2021

CMAR

View full text Add to dashboard Cite

show abstract

“…The Long non-coding RNA UCA1 was located in chromosome 9p13.12, and has been found to be overexpressed in tumor tissues, such as esophageal squamous cell carcinoma,colorectal cancer, ovarian cancer, bile duct carcinoma and melanoma etc. [16][17][18][19][20][21][22][23].UCA1 are participated in the tumorigenesis and progression, functioning as an oncogene [24][25][26][27][28][29][30]. However, the relation between UCA1 and renal cancer is still unknown and mysterious particularly.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulated evidences indicate the reciprocal inhibition between lncRNAs and miRNAs [16,20,22,24,25,Fig. 9 UCA1 positively regulates DLL4 expression via sponging miR-182-5p.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidences suggested that long non-coding RNAs (lncRNAs) perform important or vital functions in the malignant tumors [9][10][11][12][13][14][15]. LncRNA urothelial cancer associated 1 (UCA1) is abnormally expressed in esophageal squamous cell carcinoma, colorectal cancer, gastric cancer melanoma cells, pancreatic cancer, thyroid cancer, lung cancer and so on [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. In vitro and in vivo assays were conducted to further explore its underlying roles in tumor progression.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

101

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

“…Taken together, these results indicated that LINC01089 acts as a metastasisinhibiting marker during NSCLC progression, consistent with the function previously reported in breast cancer. One of the major mechanisms for lncRNAs is that they function as competing endogenous RNA, where they bind miRNAs and generate a posttranscriptional function in mRNA targets associated with tumorigenesis (20)(21)(22)(23). In the present study, we determined whether LINC01089 functions as a competing endogenous RNA in NSCLC by analyzing its subcellular localization in cell line.…”

Section: Linc01089 Suppresses Emt In Nsclc Via the Mir-27a-sfrp1-wnt/mentioning

confidence: 93%

LINC01089 Inhibits Tumorigenesis and Epithelial–Mesenchymal Transition of Non-small Cell Lung Cancer via the miR-27a/SFRP1/Wnt/β-catenin Axis

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) have emerged as regulators of gene expression and play critical regulatory roles in diverse biological functions and diseases, including cancer. In this study, we report the downregulation of LINC01089 in non-small cell lung cancer (NSCLC) samples, relative to adjacent non-tumor tissues, and demonstrate its role in the inhibition of proliferation, migration, and epithelial–mesenchymal transition (EMT) of NSCLC cells. Mechanistic analysis indicates that LINC01089 acts as a sponge for miR-27a, regulating its expression in NSCLC. Interestingly, LINC01089 mediated the upregulation of SFRP1 expression by inhibiting the Wnt/β-catenin–EMT pathway and inhibiting the epithelial–mesenchymal transition of NSCLC via sponging miR-27a. Overall, our findings highlight LINC01089’s tumorigenic role and regulatory mechanism in NSCLC, thereby suggesting its potential as a therapeutic target for managing NSCLC.

show abstract

Long noncoding RNA UCA1 enhances sensitivity to oncolytic vaccinia virus by sponging miR-18a/miR-182 and modulating the Cdc42/filopodia axis in colorectal cancer

Cited by 20 publications

References 23 publications

LncRNA UCA1 Enhances Cisplatin Resistance by Regulating CYP1B1-mediated Apoptosis via miR-513a-3p in Human Gastric Cancer

LncRNA UCA1 Enhances Cisplatin Resistance by Regulating CYP1B1-mediated Apoptosis via miR-513a-3p in Human Gastric Cancer

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

LINC01089 Inhibits Tumorigenesis and Epithelial–Mesenchymal Transition of Non-small Cell Lung Cancer via the miR-27a/SFRP1/Wnt/β-catenin Axis

Contact Info

Product

Resources

About