The Targeting Mechanism of Long Intergenic Non-Coding RNA 01503 to miR-338-3p and Its Regulation on Cell Behaviors of Bladder Cancer T24 Cells

2021 ◽  
Vol 11 (7) ◽  
pp. 1406-1412
Author(s):  
Tingming Wu ◽  
Shibao Fu ◽  
Shuming He ◽  
Xianping Che ◽  
Zhibo Mo
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Ki 67 ◽  
Cell Behaviors ◽  
T24 Cells ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Bladder Cancer Cells ◽  
Protein Expressions

This study aimed to investigate the effects of long intergenic non-coding RNA 01503 (LINC01503) on cell behaviors of T24 bladder cancer cells, including proliferation and apoptosis, as well as its mechanism for targeting miR-338-3p. First, bladder cancer tissues and the corresponding adjacent tissues were obtained and subjected to RT-qPCR to analyze their LINC01503 and miR-338-3p expressions. Afterward, si-LINC01503, miR-338-3p mimics were transfected into T24 cells and then CCK-8 assay and flow cytometry were applied to analyze the cell behaviors of the T24 cells, including proliferation and apoptosis. In additionally, Western blot was carried out to analyze the protein expressions of Ki-67, Bcl-2, and Bax. Finally, dual luciferase reporter and RT-qPCR assay were used to confirm the targeted function of LINC01503 to miR-338-3p. Our data clearly demonstrates a highly expressed LINC01503 and a lowly expressed miR-338-3p in bladder cancer. Interfering LINC01503 was found to obviously influence some protein expressions, such that it down-regulated Ki-67 and Bcl-2 expressions, but upregulated Bax expression, thus resulting in reduced proliferation and enhanced apoptosis. Meanwhile, miR-338-3p overexpression was found to influence these protein expressions, which was similar to functions of the interfering LINC01503. Furthermore, it was found that LINC01503 directly binds to miR-338-3p and that LINC01503 overexpression could obviously down-regulate miR-338-3p expression, thus weakening the influence of interfering LINC01503 on behaviors of the T24 cells. Our results demonstrate that interfering LINC01503 could affect cell behaviors of T24 bladder cancer cells, inhibit proliferation, and induce apoptosis, which was mediated by the targeted binding of interfering LINC01503to miR-338-3p.

scholarly journals LINC00511/miRNA-143-3p Modulates Apoptosis and Malignant Phenotype of Bladder Carcinoma Cells via PCMT1

2021 ◽  
Vol 9 ◽  
Author(s):  
Li-Ming Dong ◽  
Xi-Ling Zhang ◽  
Ming-Huan Mao ◽  
Yan-Pei Li ◽  
Xi-Yan Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Clinicopathological Parameters ◽  
Regulation Mechanism ◽  
Luciferase Reporter Gene ◽  
Non Coding Rna ◽  
Bladder Cancer Cells ◽  
The Relationship

Bladder cancer has easy recurrence characteristics, but its occurrence and development mechanism are still unclear. Non-coding RNA is a kind of RNA that exists widely and cannot be translated into proteins, which has played a key role in the regulation of biological functions of tumor cells. However, the regulation mechanism of non-coding RNA on bladder tumors is not fully understood. By microarray analysis and database analysis, we found that LINC00511 was significantly highly expressed in bladder cancer. The expressions of LINC00511, miR-143-3p, and PCMT in bladder cancer tissues and cells were detected by quantitative reverse transcription–polymerase chain reaction. The relationship between the expressions of miR-143-3p and PCMT1 and the clinicopathological parameters of the tumor was analyzed. The proliferation and invasion of bladder cancer cells were detected by MTT assay and Transwell assay. The expression levels of E-cadherin and vimentin in bladder cancer cells were detected by Western blot. Cell apoptosis was detected by flow cytometry. In vivo, TCCSUP or SW780 cells were inoculated into BALB/c nude mice to detect tumor volume and weight. Bioinformatics and dual luciferase reporter gene were used to analyze the relationship between LINC00511 and miR-143-3p and its downstream target gene PCMT1. The results showed that LINC00511 could target miR-143-3p/PCMT1 to regulate the proliferation, migration, and apoptosis of bladder cancer TCCSUP or SW780 cells and promote the occurrence and development of bladder cancer.

scholarly journals The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

2017 ◽  
Vol 43 (1) ◽  
pp. 405-418 ◽  
Author(s):  
Yaoyao Xiong ◽  
Long Wang ◽  
Yuan Li ◽  
Minfeng Chen ◽  
Wei He ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Cancer Growth ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
Bladder Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

scholarly journals Long non-coding RNA SOX2OT promotes the stemness phenotype of bladder cancer cells by modulating SOX2

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Yonghao Zhan ◽  
Zhicong Chen ◽  
Shiming He ◽  
Yanqing Gong ◽  
Anbang He ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Non Coding Rna ◽  
Bladder Cancer Cells ◽  
Long Non Coding Rna

The role of HIF-1α in regulating NLRP3 inflammasome activation in bladder cancer.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17028-e17028 ◽  
Author(s):  
Yuan-Ru Chen ◽  
Hsin-Chih Yeh ◽  
Fang-Yen Chiu ◽  
Hsin-En Wu ◽  
Huei-Chen Fang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Urothelial Carcinoma ◽  
Cancer Cells ◽  
Nlrp3 Inflammasome ◽  
Migration And Invasion ◽  
Inflammasome Activation ◽  
T24 Cells ◽  
Nlrp3 Inflammasome Activation ◽  
Bladder Cancer Cells

e17028 Background: Bladder cancer is one of the most common malignancies of urinary system with the forth incidence rate and the eighth leading mortality rate in male genitourinary tumors. Hypoxia environment activates the hypoxia‐signalling pathway, principally via hypoxia‐inducible transcription factors (HIF) to activate numerous target genes which mediate embryonic vascularization, metabolism, tumor angiogenesis and the other processes to supply tissues with blood and oxygen. Inflammasomes are multiprotein signal responsible for the maturation of proinflammatory cytokines IL-1β and IL-18 as well as trigger the inflammatory cell pyroptosis. Recent study showed that HIF-1α promotes NLRP3 inflammasome activation in bleomycin-induced acute lung injury. However, the role of HIF1α in regulating the progression of bladder cancer has not been examined so far. The present study aimed to investigate the effect of HIF-1α on NLRP3 inflammasome activation in urothelial carcinoma. Methods: In this research, urothelial carcinoma cell lines were treated with NLRP3 inflammasome inducers, LPS/ATP, to induce NLRP3 inflammasome activation. Results: Our preliminary results showed that both T24 and 5637 bladder cancer cells can be induced NLRP3 inflammasome activation and IL-1β secretion. In addition, hypoxia also induces the secretion of IL-1β in T24 cells. We further investigated the effect of NLRP3 inflammasome activation in modulating EMT-related protein levels, migration and invasion in bladder cancer T24 cells. Our results demonstrated that NLRP3 inflammasome activation promotes tumor growth and metastasis in bladder cancer cells. Furthermore, knockdown of HIF1α reduces both inflammatory response and migratory activity in bladder cancer. Conclusions: Collectively, these results suggest that targeting NLRP3 inflammasome might offer potential to treat hypoxic malignant tumor in bladder carcinoma.

Cantharidin Induces Apoptosis Through the Calcium/PKC-Regulated Endoplasmic Reticulum Stress Pathway in Human Bladder Cancer Cells

2015 ◽  
Vol 43 (03) ◽  
pp. 581-600 ◽  
Author(s):  
Chin-Chuan Su ◽  
Shing-Hwa Liu ◽  
Kuan-I Lee ◽  
Kou-Tong Huang ◽  
Tien-Hui Lu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Human Bladder Cancer ◽  
Calpain Activity ◽  
Human Bladder ◽  
T24 Cells ◽  
Bladder Cancer Cells ◽  
Human Bladder Cancer Cells ◽  
Stress Pathway

Bladder cancer is a common malignancy worldwide. However, there is still no effective therapy for bladder cancer. In this study, we investigated the cytotoxic effects of cantharidin [a natural toxin produced (pure compound) from Chinese blister beetles (Mylabrisphalerata or Mylabriscichorii) and Spanish flies (Cantharis vesicatoria)] in human bladder cancer cell lines (including: T24 and RT4 cells). Treatment of human bladder cancer cells with cantharidin significantly decreased cell viability. The increase in the expressions of caspase-3 activity and cleaved form of caspase-9/-7/-3 were also increased in cantharidin-treated T24 cells. Furthermore, cantharidin increased the levels of phospho-eIF2α and Grp78 and decreased the protein expression of procaspase-12, which was accompanied by the increase in calpain activity in T24 cells. Cantharidin was capable of increasing the intracellular Ca 2+ and the phosphorylation of protein kinase C (PKC) in T24 cells. The addition of BAPTA/AM (a Ca 2+ chelator) and RO320432 (a selective cell-permeable PKC inhibitor) effectively reversed the increase in caspase-3 and calpain activity, the phosphorylation levels of PKC and eIF2α and Grp78 protein expression, and the decrease in procaspase-12 expression induced by cantharidin. Importantly, cantharidin significantly decreased the tumor volume (a dramatic 71% reduction after 21 days of treatment) in nude mice xenografted with T24 cells. Taken together, these results indicate cantharidin induced human bladder cancer cell apoptosis through a calcium/PKC-regulated ER stress pathway. These findings suggest that cantharidin may be a novel and potential anticancer agent targeting on bladder cancer cells.

scholarly journals Knockdown of Ki-67 by Dicer-Substrate Small Interfering RNA Sensitizes Bladder Cancer Cells to Curcumin-Induced Tumor Inhibition

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e48567 ◽  
Author(s):  
Sivakamasundari Pichu ◽  
Swapna Krishnamoorthy ◽  
Andrei Shishkov ◽  
Bi Zhang ◽  
Peter McCue ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Ki 67 ◽  
Tumor Inhibition ◽  
Bladder Cancer Cells ◽  
Interfering Rna
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