scholarly journals Long non‑coding RNA H19 promotes the migration and invasion of colon cancer cells via MAPK signaling pathway

2018 ◽  
Author(s):  
Weiwei Yang ◽  
Rajkumar Redpath ◽  
Chongyou Zhang ◽  
Ning Ning
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The significance of homeodomain transcription factor 2 in colon cancer cells

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yang He ◽  
Peng Gong ◽  
Sitong Wang ◽  
Qing Xu ◽  
Jianhua Chen
Keyword(s):  
Cervical Cancer ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Homeodomain Transcription Factor ◽  
Non Coding Rna ◽  
Related Proteins ◽  
Long Non Coding Rna

Abstract Background Colon cancer is a serious malignant tumor. It has been reported that paired-like homeodomain transcription factor 2 (PITX2) can promote the progression of several types of cancer via regulating the Wnt/β-catenin pathway. It has also been demonstrated that high levels of long non-coding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) can also promote the development of cervical cancer via activating the Wnt/β-catenin pathway. However, whether PITX2 can affect the development of colon cancer via regulating the expression of lncRNA GHET1 remains unclear. Results The results demonstrated that PITX2 knockdown attenuated the proliferation, migration and invasion abilities of colon cancer cells. Additionally, PITX2 promoted the expression of lncRNA GHET1 via binding to its promoter. Overexpression of lncRNA GHET1 induced the expression of Wnt/β-catenin signaling-related proteins, cyclin D1, c-Myc and MMP-7. Furthermore, lncRNA GHET1 overexpression abrogated the PITX2 silencing-mediated decreased proliferation, migration and invasion abilities of colon cancer cells. Conclusion The findings of the present study suggested that PITX2 could enhance the proliferation, migration and invasion abilities of colon cancer cells via upregulating lncRNA GHET1 and activating the Wnt/β-catenin pathway.

Targeting of super-enhancers and mutant BRAF can suppress growth of BRAF -mutant colon cancer cells via repression of MAPK signaling pathway

2017 ◽  
Vol 402 ◽  
pp. 100-109 ◽  
Author(s):  
Yoshiaki Nakamura ◽  
Naoko Hattori ◽  
Naoko Iida ◽  
Satoshi Yamashita ◽  
Akiko Mori ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Colon Cancer Cells ◽  
Braf Mutant ◽  
Mutant Braf

scholarly journals Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway

2016 ◽  
Vol 40 (3-4) ◽  
pp. 644-656 ◽  
Author(s):  
Danni Wang ◽  
Danbo Wang ◽  
Ning Wang ◽  
Zaiqiu Long ◽  
Xuemei Ren
Keyword(s):  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Migration And Invasion ◽  
Erk Mapk ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background/Aims: Microarray screening had found BRAF-activated non-coding RNA (BANCR) was significantly upregulated in type 1 endometrial cancer (EC). This study aimed to assess the potential role of long non-coding RNA (lncRNA) BANCR in the pathogenesis and progression of type 1 EC. Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to confirm the expression of BANCR in type 1 EC tissue, and analyze its clinical significance. In vitro, RNA interference (siRNA) was used to investigate the biological role of BANCR in type 1 EC. Results: qRT-PCR revealed that the expression of lncRNA BANCR was higher in type 1 EC (P<0.01). BANCR expression was significantly correlated with FIGO stage, pathological grade, myometrial invasion, and lymph node metastasis. The expression of BANCR was significantly correlated with that of MMP2/MMP1. In vitro, knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression. Conclusion: BANCR is highly expressed in type 1 EC tissue and promotes EC-cell proliferation, migration, and invasion by activating ERK/MAPK signaling pathway that regulates MMP2/MMP1 expression. BANCR is expected to become a prognostic marker and therapeutic target in type 1 EC.

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.

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