Down-regulation LncRNA-SNHG15 Contributes to Proliferation and Invasion of Bladder Cancer Cells

2021 ◽  
Author(s):  
Aldhabi Mokhtar ◽  
Chuize Kong ◽  
Zhe Zhang ◽  
Yan Du
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Tumor Size ◽  
Tumor Stage ◽  
Rt Pcr ◽  
Down Regulation ◽  
Statistical Graph ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract OBJECTIVES: This study aimed to investigate effect of lncRNA-SNHG15 in bladder carcinoma using cell lines experiments and the relationship between clinical characteristics and lncRNA-SNHG15 expression was analyzed.Methods. Bladder cancer tissues and near-cancer tissues were collected. The expression of lncRNA-SNHG15 in tissues and cell lines was detected by real-time PCR (RT-PCR). The expression of lncRNA-SNHG15 was downregulated by interference (siRNA) as detected by RT-PCR that was used to detect the interference efficiency. CCK-8, and Transwell assays were used to evaluate the effect of lncRNA-SNHG15 on the proliferation, invasion capa­bility of bladder cancer cells.t-test was used for Statistical analyses, were performed using the Statistical Graph pad 8.0.1.224 software.Result: The expression of lncRNA-SNHG15 was up regulated in 5637, UMUC3 and T24 cell lines compared with corresponding normal controls (P<0.05). up regulation was positively related to tumor stage (P = 0.015), and tumor size (P =0.0465) . The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion.Conclusion: This study showed that lncRNA-SNHG15 is overexpressed in bladder cancer tissues and (5637, UMUC3 T24) cell lines. up regulation was positively related to tumor stage (P = 0.015), and tumor size (P =0.0465) .The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion, which provides a potential molecular target for future tumor targeted therapy.

scholarly journals Down-regulation LncRNA-SNHG15 contributes to proliferation and invasion of bladder cancer cells

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Aldhabi Mokhtar ◽  
Chuize Kong ◽  
Zhe Zhang ◽  
Yan Du
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Tumor Stage ◽  
Rt Pcr ◽  
Down Regulation ◽  
Bladder Cancer Cells ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Objectives The aim of this study was to investigate the effect of lncRNA-SNHG15 in bladder carcinoma using cell lines experiments and the relationship between clinical characteristics and lncRNA-SNHG15 expression was analyzed. Methods Bladder cancer tissues and near-cancer tissues were collected. The real-time PCR (RT-PCR) was used to detect the expression of lncRNA-SNHG15 in tissues and cell lines. The expression of lncRNA-SNHG15 was downregulated by interference (siRNA), as detected by RT-PCR, that was used to determine the efficiency of the interference. CCK-8 and Transwell assays were used to evaluate the effect of lncRNA-SNHG15 on the proliferation and invasion capability of bladder cancer cells. The t-test was used for Statistical analyses, which were carried out using the Statistical Graph pad 8.0.1.224 software. Result The expression of lncRNA-SNHG15 was up regulated in 5637, UMUC3 and T24 cell lines compared with corresponding normal controls (P < 0.05). Up regulation was positively related to tumor stage (P = 0.015). And tumor size (P = 0.0465). The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion. Conclusion This study showed that lncRNA-SNHG15 is overexpressed in bladder cancer tissues and (5637, UMUC3 T24) cell lines. Up regulation was positively related to tumor stage (P = 0.015), and tumor size (P = 0.0465). Down-regulation of lncRNA-SNHG15 by siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion, indicating a potential molecular target for future tumor targeted therapy.

scholarly journals Hsa_circ_0026134 expression promoted TRIM25- and IGF2BP3-mediated hepatocellular carcinoma cell proliferation and invasion via sponging miR-127-5p

2020 ◽  
Vol 40 (7) ◽  
Author(s):  
Wei Zhang ◽  
Liang Zhu ◽  
Guowei Yang ◽  
Bo Zhou ◽  
Jianhua Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Down Regulation ◽  
Mrna Binding Protein ◽  
New Treatment ◽  
Mrna Binding ◽  
Proliferation And Invasion

Abstract Increasing evidence shows that circular RNAs (circRNAs) play a regulatory role in cancer. In the present study, we aimed to investigate the characteristics and effects of hsa_circ_0026134 in hepatocellular carcinoma (HCC). We investigated hsa_circ_0026134 expression in 20 pairs of clinical tissues from HCC patients; expression of hsa_circ_0026134 in different cell lines; effect of hsa_circ_0026134 on proliferation and invasion of HCC cell lines; and the regulatory mechanisms and interactions among hsa_circ_0026134, miR-127-5p, tripartite motif-containing protein 25 (TRIM25) and insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3). hsa_circ_0026134 expression was increased in HCC samples and cell lines. Down-regulation of hsa_circ_0026134 attenuated HCC cell proliferation and metastatic properties. Micro (mi)RNA (miR)-127-5p was sponged by hsa_circ_0026134. Rescue experiments indicated that inhibition of miR-127-5p expression promoted cell proliferation and invasion even after hsa_circ_0026134 silencing. TRIM25 and IGF2BP3 were targets of miR-127-5p. Overexpression of TRIM25 or IGF2BP3 promoted cell proliferation and invasion in cells overexpressing miR-127-5p. Down-regulation of hsa_circ_0026134 suppressed TRIM25- and IGF2BP3-mediated HCC cell proliferation and invasion via promotion of miR-127-5p expression, which have been confirmed by luciferase reporter assay. The present study provides a new treatment target for HCC.

scholarly journals Knock Down of LINC00504 Represses Proliferation and Invasion via Regulation of miR-140-5p in Breast Cancer

2020 ◽  
Author(s):  
Tieying Hou ◽  
Long Ye ◽  
Qingsong Qin ◽  
Shulin Wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background: Breast cancer is one of the most common cancer in the world. Emerging evidence has demonstrated the critical role of long noncoding RNAs (lncRNAs) in the development of breast cancer. In this study, we aimed to investigate the role of LINC00504 in breast cancer progression. Methods: Quantification real-time PCR was used to analyzed the expression levels of LINC00504 and miR‐140-5p in breast cancer tissues and cell lines. Cell proliferation, migration and invasion were assessed by Cell Counting Kit‐8, transwell assay and Immunofluorescence. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were performed to verify the interaction between LINC00504 and miR‐140-5p. The expression levels of VEGFA, CDH1 and VIM were demonstrated by western blot assays. Result: Here, we found that LINC00504 is up regulated in breast cancer tissues and cell lines. Down regulation of LINC00504 mediated by shRNA suppressed the proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Furthermore, LINC00504 was found to competitively regulate miR‐140-5p via targeting VEGFA. Inhibition of miR‐140-5p attenuated the knockdown-LINC00504 induced inhibition of breast cancer cell proliferation and invasion.Conclusion: Taken together, our results demonstrated the mechanism of the LINC00504–miR‐140-5p–VEGFA axis in breast cancer cell proliferation and invasion and may lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

scholarly journals Downregulated Long Noncoding RNA PART1 Inhibits Proliferation and Promotes Apoptosis in Bladder Cancer

2019 ◽  
Vol 18 ◽  
pp. 153303381984663 ◽  
Author(s):  
Xin Hu ◽  
Hefei Feng ◽  
Huaxing Huang ◽  
Wei Gu ◽  
Qiuyu Fang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Ribonucleic Acid ◽  
Cell Apoptosis ◽  
Bladder Cancer Cell ◽  
Proliferation And Apoptosis ◽  
Proliferation And Invasion

Objective: In this study, we aimed to clarify the effects of long noncoding ribonucleic acid prostrate androgen-regulated transcript-1 on bladder cancer cell proliferation and apoptosis. Methods: Microarrays were implemented to investigate the long noncoding ribonucleic acid expression profiles in bladder cancer tissue (N = 9) and in noncancer bladder tissue (N = 5). Relative prostrate androgen-regulated transcript-1 expression levels in tissue samples or cell lines were detected by real-time quantitative reverse transcription-polymerase chain reaction. Prostrate androgen-regulated transcript-1 expression was enhanced by the transfection of pcDNA3.1-prostrate androgen-regulated transcript-1 and downregulated by the infection with pcMV-sh prostrate androgen-regulated transcript-1. Additionally, cell proliferation and apoptosis were measured by the cell counting kit-8 assay and flow cytometry, respectively. Cell invasion was determined by a Transwell assay. Results: Prostrate androgen-regulated transcript-1 expression was upregulated in bladder cancer tissues compared to adjacent nontumor tissues. Furthermore, prostrate androgen-regulated transcript-1 levels were successfully upregulated by pcDNA3.1-prostrate androgen-regulated transcript-1 and depleted by pCMV-sh prostrate androgen-regulated transcript-1 in bladder cancer cell lines (5637, T24). Enhanced prostrate androgen-regulated transcript-1 expression promoted cell proliferation and invasion and inhibited cell apoptosis. However, knockdown of prostrate androgen-regulated transcript-1 expression inhibited cell proliferation and invasion and induced cell apoptosis. Conclusion: In summary, these data suggest that the knockdown of prostrate androgen-regulated transcript-1 represents a tumor suppressor player in bladder cancer and contributes to the inhibition of tumor proliferation, the promotion of cell apoptosis, and the suppression of cell invasion. Prostrate androgen-regulated transcript-1 may function as a new prognostic biomarker and as a feasible therapeutic target for patients with bladder cancer.

scholarly journals LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer

2021 ◽  
Author(s):  
Xuefeng Xing ◽  
Ming An ◽  
Tonghua Chen
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Luciferase Reporter ◽  
Cancer Cell Proliferation ◽  
Transfected Cells ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear. Objective The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer. Methods The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms. Results SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells. Conclusions SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.

Long non-coding RNA MIAT promotes cervical cancer proliferation and migration

2020 ◽  
Vol 168 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Lei Zhang ◽  
Shuxia Ge ◽  
Bing Cao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Model ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Abstract Cervical cancer is one of the most common cancers in the world while its pathological mechanisms are not well-elucidated. Long non-coding RNA (lncRNA) has been implicated in cancer development. The dysregulation of lncRNA myocardial infarction-associated transcript (MIAT) has been reported in several cancers while its role in cervical cancer is not described yet. In this study, the role of MIAT in cervical cancer was explored. We evaluated the expression of MIAT in cervical cancer tissues and cell lines. Furthermore, we explored the effects of MIAT on proliferation and invasion of cervical cancer using cell model and animal transplantation model. We also evaluated the effects of MIAT on activation of PI3K/Akt/mTOR signalling pathway. Our results show that MIAT was up-regulated in cervical cancer tissues and cell lines. Knocking down MIAT resulted in decreased cell proliferation, migration and invasion of cervical cancer cells and suppression of tumour growth in mice. Mechanically, knocking down MIAT suppressed the activation of PI3K/Akt signalling pathway. In conclusion, MIAT promotes cell proliferation and invasion in cervical cancer.

scholarly journals Linc00887 suppresses tumorigenesis of cervical cancer through regulating the miR-454-3p/FRMD6-Hippo axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Pei Li ◽  
Jinsheng Wang ◽  
Lingran Zhi ◽  
Fengmei Cai
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Hippo Signaling ◽  
Luciferase Reporter Gene ◽  
Hippo Signaling Pathway ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background Emerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown. Methods In vivo or vitro, RT-qPCR assay was used to detect the expression of linc00887 in human normal (N = 30), cervical cancer tissues (N = 30), human normal cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (HeLa, C33A). Then, CCK-8 and Transwell assays were used to examine cell proliferation and invasion when linc00887 was overexpressed or knocked down. In addition, bioinformatics, luciferase reporter gene and pull-down assays were used to predict and validate the relationship between linc00887 and miR-454-3p. Moreover, we detected the expression of miR-454-3p in Ect1/E6E7, HeLa and C33A cells when linc00887 was overexpressed or knocked down. Cell proliferation and invasion were also measured when pcDNA-linc00887 and miR-454-3p were transfected alone or together. Next, miR-454-3p target gene was predicted and validated by bioinformatics and luciferase reporter gene assays. Gain- and loss-of-function experiments were performed in HeLa cells to evaluate the effect of miR-454-3p or linc00887 on the expression of FERM domain containing protein 6 (FRMD6) protein and several key proteins in the FRMD6-Hippo signaling pathway. Results Linc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway. Conclusions Linc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.

scholarly journals Knock Down of LINC00504 Represses Proliferation and Invasion via Regulation of miR-140-5p in Breast Cancer

2020 ◽  
Author(s):  
tieying hou ◽  
long ye ◽  
qingsong qin ◽  
shulin wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background: Breast cancer is one of the most common cancer in the world. Emerging evidence has demonstrated the critical role of long noncoding RNAs (lncRNAs) in the development of breast cancer. In this study, we aimed to investigate the role of LINC00504 in breast cancer progression. Methods: Quantification real-time PCR was used to analyzed the expression levels of LINC00504 and miR‐140-5p in breast cancer tissues and cell lines. Cell proliferation, migration and invasion were assessed by Cell Counting Kit‐8, transwell assay and Immunofluorescence. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were performed to verify the interaction between LINC00504 and miR‐140-5p. The expression levels of VEGFA, CDH1 and VIM were demonstrated by western blot assays. Result: Here, we found that LINC00504 is up regulated in breast cancer tissues and cell lines. Down regulation of LINC00504 mediated by shRNA suppressed the proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Furthermore, LINC00504 was found to competitively regulate miR‐140-5p via targeting VEGFA. Inhibition of miR‐140-5p attenuated the knockdown-LINC00504 induced inhibition of breast cancer cell proliferation and invasion. Conclusion: Taken together, our results demonstrated the mechanism of the LINC00504–miR‐140-5p–VEGFA axis in breast cancer cell proliferation and invasion and may lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

scholarly journals CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer

2021 ◽  
Vol 7 ◽  
Author(s):  
Zhongfu Zhang ◽  
Jieqing Chen ◽  
Zhongshuang Zhu ◽  
Zhongqing Zhu ◽  
Xinhui Liao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Negative Control ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Novel Target ◽  
Induced Apoptosis ◽  
Cancer Tissues ◽  
E Cadherin

The current study is to investigate the expression pattern and biological function of long non-coding RNA Focally gastric cancer-associated transcript3 (GACAT3) in bladder cancer. Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues. Human bladder cancer T24 and 5637 cell lines were transiently transfected with specific CRISPR-Cas13 or negative control CRISPR-Cas13. Cell migration, proliferation, and apoptosis were measured by using wound healing assay CCK-8 assay and Caspase-3 ELISA assay, respectively. The expression changes of p21, Bax, and E-cadherin after knockdown of GACAT3 were detected by using Western blot. The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues. Inhibition of cell proliferation, increased apoptosis, and decreased motility were observed in T24 and 5637 cell lines transfected by CRISPR-Cas13 targeting GACAT3. Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3. A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT3 may be a novel target for diagnosis and treatment of bladder cancer.

scholarly journals Circ_0071662, a novel tumor biomarker, suppresses bladder cancer cell proliferation and invasion by sponging miR-146b-3p

2019 ◽  
Author(s):  
Rena Abulizi ◽  
Bo Li ◽  
Chuan-guang Zhang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Tumor Biomarker ◽  
Cancer Cell Proliferation ◽  
Human Bladder ◽  
Bladder Cell ◽  
Proliferation And Invasion

Here, we characterized a new circRNA, named circ_0071662, which was downregulated in human bladder cancer tissues and cell lines, compared with matched adjacent normal tissues and normal bladder epithelial cells. Lower circ_0071662 level was observed in patients with advanced bladder cancer and was positively associated with poorer prognosis, including higher degrees of lymph node invasion and distal metastasis, and lower survival rate. Gain- and loss-of-functions showed that circ_0071662 suppressed cell proliferation and invasion in human bladder cell lines T-24 and J82. Bioinformatics analysis revealed that there are six binding sites of miR-146b-3p on circ_0071662 sequence, and pull-down assays demonstrated miR-146b-3p directly bound with circ_0071662. Moreover, circ_0071662 negatively regulated miR-146b-3p expression and positively regulated expression of miR-146b-3p target genes HPGD and NF2. Furthermore, miR-146b-3p could rescue the inhibition of cell proliferation and invasion caused by circ_0071662 overexpression. In conclusion, circ_0071662 suppresses bladder cancer cell proliferation and invasion by sponging miR-146b-3p.

Sign in / Sign up

Export Citation Format

Share Document