LncRNA BANCR Promotes Pancreatic Cancer Tumorigenesis via Modulating MiR-195-5p/Wnt/β-Catenin Signaling Pathway

Wu, Xianping; Xia, Tianfang; Cao, Meng; Zhang, Pengbo; Shi, Guodong; Chen, Lei; Zhang, Jingjing; Yin, Jie; Wu, Pengfei; Cai, Baobao; Lu, Zipeng; Miao, Yi; Jiang, Kuirong

doi:10.1177/1533033819887962

Cited by 40 publications

(32 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…31 Wu et al demonstrated that BRAF-activated noncoding RNA promotes tumorigenesis of pancreatic cancer by sponging miR-195. 32 Overall, our results demonstrated that SNHG12 could accelerate tumorigenesis of DLBCL cells through miR-195 sponging.…”

Section: Discussionmentioning

confidence: 57%

<p>Long Noncoding RNA SNHG12 Indicates the Prognosis and Accelerates Tumorigenesis of Diffuse Large B-Cell Lymphoma Through Sponging microR-195</p>

Chen¹,

Zhang²,

Han³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Small nucleolar RNA host gene 12 (SNHG12) expression is associated with multiple cancers, including renal cell carcinoma, prostate cancer, cervical cancer, nasopharyngeal carcinoma, colorectal cancer, and hepatocellular carcinoma. However, SNHG12 biological function is unclear in diffuse large B-cell lymphoma (DLBCL). Methods: SNHG12 expression and associated clinicopathological characteristics were evaluated in DLBCL tissues. CCK-8 and transwell assay were used to analyze the in vitro role of SNHG12 in DLBCL progression. The xenograft model was used to explore the in vivo role of SNHG12 in DLBCL growth. The physical interaction between SNHG12 and miR-195 was confirmed using bioinformatics analysis and a dual luciferase assay. Results: SNHG12 expression was upregulated in DLBCL tissues and correlated with patients' prognosis. SNHG12 downregulation inhibited cell growth, migration, and invasion of DLBCL cells in vitro, while its overexpression promoted these cellular processes. Moreover, SNHG12 knockdown repressed tumorigenesis of DLBCL cells in vivo. Further experiments demonstrated that miR-195 is a target of SNHG12 in DLBCL and that their expression negatively correlates in DLBCL. SNHG12 functioned as a competing endogenous RNA for miR-195 in DLBCL cells and miR-195 upregulation abolished the effects of SNHG12 on of DLBCL progression. Conclusion: SNHG12 predicts poor clinical outcome and serves as a novel oncogene in DLBCL via miR-195 sponging. We also suggest that SNHG12 can be used as a potential therapeutic candidate for DLBCL patients.

show abstract

Section: Discussionmentioning

confidence: 57%

<p>Long Noncoding RNA SNHG12 Indicates the Prognosis and Accelerates Tumorigenesis of Diffuse Large B-Cell Lymphoma Through Sponging microR-195</p>

Chen¹,

Zhang²,

Han³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…The function of the Wnt/β-catenin pathway on EC growth had been well-established (18). β-Catenin maintains epithelial cell integrity, an important barrier for blocking tumor metastasis (19). Additionally, hypophosphorylated β-catenin transfers into the nucleus and binds to transcription factors, leading to transcriptional activation of specific target genes, including Cyclin D1, C-MYC, and MMP-7, all of which contribute to cell survival, cell cycle, uncontrolled proliferation, and distant metastasis (20).…”

Section: Introductionmentioning

confidence: 99%

Ubiquitin C-Terminal Hydrolase L5 (UCHL5) Accelerates the Growth of Endometrial Cancer via Activating the Wnt/β-Catenin Signaling Pathway

et al. 2020

View full text Add to dashboard Cite

Endometrial cancer (EC) is the most prevalent gynecological malignancy with high mortality. Chemotherapy plays a pivotal role both in an adjuvant setting and in exclusive treatment. However, current pharmacotherapies are limited and not ideal for improving the overall survival of EC patients. Thus, identification of the underlying molecular mechanisms responsible for initiation and progression of EC is imperative for developing novel therapeutic strategies. Ubiquitin C-terminal hydrolase L5 (UCHL5) has been found to aggravate tumor growth and metastasis in several different types of tumor models such as esophageal squamous cell carcinoma, hepatocellular carcinoma, and epithelial ovarian cancer. However, whether UCHL5 influences the growth of EC has not been elucidated. To expose the role of UCHL5 on EC, bioinformatics analysis was conducted, and it hinted that UCHL5 was overexpressed in EC tissues and associated with lower overall survival. Consistently, the overexpression of UCHL5 in EC tissues and cell lines was further confirmed by western blot (WB) and polymerase chain reaction (PCR) compared with non-tumor control. Lentivirus vectors carrying UCHL5 shRNA or CD sequences were used to reduce or overexpress the UCHL5 gene, respectively. Cell proliferation and cycle were facilitated, and cell apoptosis was decreased when the UCHL5 gene was overexpressed in EC cell lines. These results were opposite in UCHL5 knockdown EC cells. Additionally, the expression of β-catenin is positively related to UCHL5 levels and the tumorigenic effects of UCHL5 overexpression were reversed by the Wnt/β-catenin pathway inhibitor XAV939. Thus, Wnt/β-catenin pathway activation may be a partial mechanism responsible for the promoting effects of UCHL5 on EC growth. In conclusion, UCHL5 accelerated the growth of EC via the Wnt/β-catenin pathway and was expected to be an attractive target for EC treatment.

show abstract

“…However, treatments limited to chemotherapy associated with resistance development do not re ect well on patients who defy surgical resection, carrying with primary migration, or diseases with high recurrence [29]. Accumulating researches have shown that lncRNA is an essential cell regulator in tumor progression, including osteosarcoma, which brings new ideas for the treatment of osteosarcoma [30][31][32]. This study rst explored a new lncRNA, namely LINC00485.…”

Section: Discussionmentioning

confidence: 99%

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

Hu¹,

Luo²,

Zhou³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Mounting researches have established that long-chain non-coding RNA (lncRNA) and microRNA (miRNA) occupy an essential position in osteosarcoma development. The present study attempted to explicate the functional role and mechanism of LINC00485 and miR-361-5p in regulating the osteosarcoma progression.Methods: RT-PCR was employed to measure LINC00485 expression in osteosarcoma tissues and adjacent healthy tissues. Moreover, the correlation between LINC00485 expression and the clinicopathological indexes was analyzed. Further, the LINC00485 low-expressed cell model was constructed, and the CCK8 assay was employed to measure cell proliferation, followed by the flow cytometry in apoptosis testing. Besides, Transwell assay was utilized to detect cell migration and invasion ability, and Western blot examined the alternations of epithelial mesenchymal transition (EMT) marker molecules (E-cadherin and Vimentin). Furthermore, bioinformatics analysis was taken advantage of predicting the downstream molecular targets of LINC00485. RT-PCR and Western blot were carried out respectively to estimate the expression variations of miR-361-5p and Twist1. Dual luciferase activity assay and RNA co-precipitation (RIP) assay were conducted to verify the targeting relationship between LINC00485 and miR-361-5p, miR-361-5p and Twist1.Results: In comparison with normal adjacent tissues, the LINC00485 expression in cancer tissues was profoundly up-regulated. LINC00485 low expression greatly attenuated proliferation, migration, invasion, and EMT in osteosarcoma cells, while enhancing apoptosis. Bioinformatics analysis claimed that miR-361-5p was a sponge miRNA for LINC00485, targeting the Twist1 expression. Further gain- and loss-experiments declared that miR-361-5p limited the osteosarcoma development by inhibiting osteosarcoma cell proliferation, metastasis and promoting apoptosis.Conclusions: LINC00485 acted as an oncogene in the osteosarcoma tumorigenesis by modulating the miR-361-5p/Twist1 axis.

show abstract

LncRNA BANCR Promotes Pancreatic Cancer Tumorigenesis via Modulating MiR-195-5p/Wnt/β-Catenin Signaling Pathway

Cited by 40 publications

References 54 publications

<p>Long Noncoding RNA SNHG12 Indicates the Prognosis and Accelerates Tumorigenesis of Diffuse Large B-Cell Lymphoma Through Sponging microR-195</p>

<p>Long Noncoding RNA SNHG12 Indicates the Prognosis and Accelerates Tumorigenesis of Diffuse Large B-Cell Lymphoma Through Sponging microR-195</p>

Ubiquitin C-Terminal Hydrolase L5 (UCHL5) Accelerates the Growth of Endometrial Cancer via Activating the Wnt/β-Catenin Signaling Pathway

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

Contact Info

Product

Resources

About