scholarly journals Cervical carcinoma high‑expressed long non‑coding RNA 1 may promote growth of colon adenocarcinoma through interleukin‑17A

2019 ◽  
Author(s):  
Jue Wang ◽  
Hui Li ◽  
Cuiying Zhang ◽  
Liying Xue ◽  
Zhihui Cai
Keyword(s):  
Cervical Carcinoma ◽  
Colon Adenocarcinoma ◽  
Interleukin 17A ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Arash Poursheikhani ◽  
Mohammad Reza Abbaszadegan ◽  
Negin Nokhandani ◽  
Mohammad Amin Kerachian
Keyword(s):  
Colon Adenocarcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Integration Analysis

scholarly journals LINC01123 facilitates proliferation, invasion and chemoresistance of colon cancer cells

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Shicai Ye ◽  
Bilan Sun ◽  
Weiyun Wu ◽  
Caiyuan Yu ◽  
Ting Tian ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Colon Adenocarcinoma ◽  
Colon Cancer Cells ◽  
Prognostic Signature ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Colon Cancer Progression ◽  
Long Non Coding Rna

Abstract Colon cancer is one of the major causes of cancer-related deaths worldwide. Long non-coding RNA (lncRNA) LINC01123 has been suggested to act as an oncogene in non-small cell lung cancer and a prognostic signature in head and neck squamous cell carcinoma. However, its role in colon cancer remains obscure. From TCGA database, LINC01123 was observed to be up-regulated in colon adenocarcinoma (COAD). Subsequently, the up-regulated LINC01123 was also detected in colon cancer cells. Functionally, LINC01123 could enhance cell proliferation, migration, invasion and angiogenesis. Moreover, the chemoresistance of colon cancer cells was verified to be promoted by LINC01123. Afterward, LINC01123 was found to bind with Ago2 and miR-34c-5p. Besides, miR-34c-5p was confirmed to inhibit the cellular process and chemoresistance of colon cancer cells. Then, VEGFA was disclosed to coexist with LINC01123 and miR-34c-5p in RNA-induced silencing complex. And TCGA database suggested that its expression was correlated with different stages of COAD. Moreover, it was uncovered that VEGFA could bind with miR-34c-5p and its expression positively correlated with LINC01123 expression. Finally, LINC01123 was proofed to regulate colon cancer progression and cells chemoresistance via VEGFA. In conclusion, LINC01123/miR-34c-5p/VEGFA axis promotes colon cancer malignancy and cells chemoresistance.

scholarly journals Long Non-Coding RNA LINC00313 Accelerates Cervical Carcinoma Progression by miR-4677-3p/CDK6 Axis

2021 ◽  
Vol Volume 14 ◽  
pp. 2213-2226
Author(s):  
Yongning Zhai ◽  
Yang Liu ◽  
Zhen Wang ◽  
Wei Wang ◽  
Juan Zhou ◽  
...  
Keyword(s):  
Cervical Carcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non‐coding RNA ZEB1‐AS1 promotes colon adenocarcinoma malignant progression via miR‐455‐3p/PAK2 axis

2019 ◽  
Vol 53 (1) ◽  
Author(s):  
Xin Ni ◽  
Yuting Ding ◽  
Haitao Yuan ◽  
Jinmin Shao ◽  
Yan Yan ◽  
...  
Keyword(s):  
Colon Adenocarcinoma ◽  
Malignant Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Knockdown of long non-coding RNA GHET1 suppresses cervical carcinoma in vitro and in vivo

2020 ◽  
Vol 28 (1) ◽  
pp. 21-32 ◽  
Author(s):  
Wang Ling ◽  
Xu Yangchun ◽  
Wang Wei ◽  
Wang Qiang
Keyword(s):  
Cervical Carcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract 1817: Differential expression of long non-coding RNA in colon adenocarcinoma RNA-sequence data set

2019 ◽  
Author(s):  
Stephen J. O'Brien ◽  
Theodore Kalbfleisch ◽  
Sudhir Srivastava ◽  
Shesh Rai ◽  
Susan Galandiuk
Keyword(s):  
Differential Expression ◽  
Sequence Data ◽  
Colon Adenocarcinoma ◽  
Data Set ◽  
Rna Sequence ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA RP11-284F21.9 functions as a ceRNA regulating PPWD1 by competitively binding to miR-769-3p in cervical carcinoma

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Hong-Fang Han ◽  
Qian Chen ◽  
Wen-Wei Zhao
Keyword(s):  
Cervical Carcinoma ◽  
Gynecological Cancer ◽  
Tumor Model ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Peptidylprolyl Isomerase

Abstract Cervical carcinoma is the most common gynecological cancer in women worldwide. Emerging evidence has shown that long non-coding RNAs (lncRNAs) participate in multiple biological processes of cervical carcinoma tumorigenesis. We aimed to investigate the function of a novel lncRNA RP11-284F21.9 in cervical carcinoma. We found that RP11-284F21.9 was down-regulated in cervical carcinoma tissues and cell lines. Overexpression of RP11-284F21.9 inhibits proliferation, invasion and migration of cervical carcinoma cells in vitro. Further, we identified that RP11-284F21.9 directly interacted with miR-769-3p and functioned as the miR-769-3p sponge. Mechanistically, we showed that miR-769-3p regulated peptidylprolyl isomerase domain and WD repeat-containing protein1 (PPWD1) expression by targeting PPWD1 3′-UTR. Furthermore, xenograft tumor model revealed that overexpression of RP11-284F21.9 inhibited tumor growth of cervical carcinoma in vivo. Taken together, our results demonstrate that RP11-284F21.9 functions as tumor suppressor and regulates PPWD1 expression through competitively binding to miR-769-3p in cervical carcinoma, suggesting that RP11-284F21.9/miR-769-3p/PPWD1 axis could serve as a promising prognostic biomarker and therapeutic target for cervical carcinoma.

scholarly journals LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qingyun Pan ◽  
Ying Huang ◽  
Yirui Wang ◽  
Deke Li ◽  
Changjiang Lei
Keyword(s):  
Cell Proliferation ◽  
Colony Formation ◽  
Colon Adenocarcinoma ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Over Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. Materials and methods The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. Results ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3ʹ untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. Conclusion Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

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