scholarly journals Kinesin Superfamily Member 18B (KIF18B) Promotes Cell Proliferation in Colon Adenocarcinoma

2020 ◽  
Vol Volume 12 ◽  
pp. 12769-12778
Author(s):  
Fei Zhao ◽  
Yunzhang Feng ◽  
Xueqiang Zhang ◽  
Xiaohui Liu ◽  
Aili Li
Keyword(s):  
Cell Proliferation ◽  
Colon Adenocarcinoma ◽  
Kinesin Superfamily

scholarly journals MicroRNA-708 targeting ZNF549 regulates colon adenocarcinoma development through PI3K/AKt pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhidong Zhao ◽  
Xianju Qin
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Colon Adenocarcinoma ◽  
Signal Pathway ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Colon adenocarcinoma (COAD) is the most common type of gastrointestinal cancer and is still the third leading cause of cancer-related mortality worldwide. Therefore, finding new and promising drugs to eradicate cancer may be a feasible method to treat COAD patients. Cys2-His2 zinc finger proteins (ZFPs) is one of the largest transcription factor family and many of them are highly involved in regulation of cell differentiation, proliferation, apoptosis, and neoplastic transformation. In this study, we identified a tumor-inhibiting factor, ZNF549, which expressed lowly in COAD tissues and COAD cell lines (HT29, HCT116, SW480, LoVo, and SW620). Overexpression of ZNF549 inhibit the ability of COAD cell proliferation and migration. On the contrary, decreasing the ZNF549 expression level promote the ability of COAD cell proliferation and migration. Through bioinformatics analysis, we found that ZNF549 was a potential target of hsa-miR-708-5p (miR-708-5p). Furthermore, we verified the possibility of miR-708-5p targeting the ZNF549 gene, and miR-708-5p inhibited the expression of ZNF549 by luciferase reporter assays, qRT-PCR and western blot assays. Moreover, the relationship between miR-708-5p and phosphatidylinositol 3-kinase/AKt (PI3K/AKt) signal pathway was elucidated. Overexpression and inhibition of miR-708-5p resulted in increased and decreased expression of p-AKt and p-PI3K in HCT116 cells, respectively. RT-qPCR and western blot assays results demonstrated that miR-708-5p regulated COAD cells development by promoting the process of Epithelial-mesenchymal transition (EMT) through PI3K/AKt signaling pathway. In summary, our findings demonstrated that ZNF549, the target gene of miR-708-5p, functions as a tumor suppressor to inhibit COAD cell lines proliferation and migration through regulate the PI3K/AKt signal pathway.

scholarly journals LncRNA ACTA2-AS1 Suppress Colon Adenocarcinoma Progression by Sponging miR-4428 Upregulation BCL2L11

2020 ◽  
Author(s):  
Qingyun Pan ◽  
Ying Huang ◽  
Yirui Wang ◽  
Deke Li ◽  
Changjiang Lei
Keyword(s):  
Cell Proliferation ◽  
Colony Formation ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Over Expression ◽  
Non Coding Rna

Abstract BackgroundLong 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 MethodsThe 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. ResultsACTA2-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. ConclusionOur data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

scholarly journals SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis

2020 ◽  
Vol 20 (5) ◽  
pp. 1-1
Author(s):  
Fu‑Ren Yue ◽  
Zhi‑Bin Wei ◽  
Rui‑Zhen Yan ◽  
Qiu‑Hong Guo ◽  
Bing Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Colon Adenocarcinoma ◽  
Proliferation And Apoptosis

scholarly journals The tsRNAs (tRFdb-3013a And tRFdb-3013b) Serve As Novel Biomarkers For Colon Adenocarcinomas

2021 ◽  
Author(s):  
Xiaoling Wu ◽  
Lihong Tan ◽  
Zhurong Tang ◽  
Chunjie Wen ◽  
Huan Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Colon Adenocarcinoma ◽  
Bioinformatic Analysis ◽  
Molecular Signature ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Diagnosis And Prognosis ◽  
Adenocarcinoma Cells ◽  
Reporter Assays ◽  
Novel Biomarkers

Abstract Background: The tsRNAs (tRNA-derived small RNAs) are novel class of small non-coding RNAs derived from transfer-RNAs. Colon adenocarcinoma (COAD) are well known malignant intestinal tumors. This study focused on the identification and characterization of tsRNA biomarkers in colon adenocarcinomas. Methods: Data processing, bioinformatic analysis and visualization were performed with R or Python software. The cell proliferation, migration and invasion ability were described by CCK-8 and transwell assays. Luciferase reporter assays were performed to test the binding of tsRNA with its target.Results: With computational approaches, we identified the tsRNA fragments profiles within COAD datasets, and discriminated forty-two differentially expressed tsRNAs between colon adenocarcinomas and non-tumor controls. Among the fragments derived from the 3′ end of mature tRNA-His-GUG (a histidyl-transfer-RNA), tRFdb-3013a and tRFdb-3013b (tRFdb-3013a/b) were significantly decreased in colon adenocarcinomas, especially, tRFdb-3013a/b may tend to down-regulated in the patients with lymphatic or vascular invasion present. The clinical survival of colon adenocarcinomas patients with low tRFdb-3013a/b expression was significantly worse than that of high expression patients. In colon adenocarcinoma cells, tRFdb-3013a could suppressed cell proliferation, and reduced cell migration and invasion ability. The enrichment analyses showed that most of tRFdb-3013a-related genes were enriched in the extracellular matrix associated GO terms, phagosome pathway, and a GSEA molecular signature. Mechanically, the 3′UTR of ST3GAL1 mRNA was predicted to contain the putative binding sites of tRFdb-3013a/b, tRFdb-3013a/b might directly target ST3GAL1 and regulate ST3GAL1 expression in colon adenocarcinomas. Conclusions: These results suggested that tRFdb-3013a and tRFdb-3013b might serve as novel biomarkers for diagnosis and prognosis of colon adenocarcinomas, and play an important role in tumor progression of colon adenocarcinomas.

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.

Sign in / Sign up

Export Citation Format

Share Document