miR-29a-3p directly targets Smad nuclear interacting protein 1 and inhibits the migration and proliferation of cervical cancer HeLa cells

Chen, Ying; Zhang, Weiji; Yan, Lijun; Zheng, Peng; Jin, Li

doi:10.7717/peerj.10148

Cited by 23 publications

(20 citation statements)

References 33 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous study pointed out that the expression of miR-29a-3p was markedly lower in prostate cancer (PCa) tissues than adjacent non-tumorous tissues and miR-29a-3p overexpression could inhibit the proliferation, migration and invasion of PCa cells [ 42 ]. Moreover, miR-29a-3p mediated its tumor-suppressive activity and suppressed the tumorigenicity in HeLa cells by directly targeting smad nuclear interacting protein 1 (SNIP1) [ 43 ]. However, there was no previous report investigated expression levels and regulatory roles of miR-29a-3p in LUAD tissues.…”

Section: Discussionmentioning

confidence: 99%

C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

Lin

et al. 2022

BMC Pulm Med

View full text Add to dashboard Cite

Objective C1QTNF6 has been implicated as an essential component in multiple cellular and molecular preliminary event, including inflammation, glucose metabolism, endothelial cell modulation and carcinogenesis. However, the biological process and potential mechanism of C1QTNF6 in lung adenocarcinoma (LUAD) are indefinite and remain to be elucidated. Therefore, we investigated the interaction among the traits of C1QTNF6 and LUAD pathologic process. Methods RT-qPCR and western blot were conducted to determine the expression levels of C1QTNF6. RNA interference and overexpression of C1QTNF6 were constructed to identify the biological function of C1QTNF6 in cellular proliferative, migratory and invasive potentials in vitro. Dual-luciferase reporter assay was applied to identify the possible interaction between C1QTNF6 and miR‐29a-3p. Moreover, RNA sequencing analysis of C1QTNF6 knockdown was performed to identify the potential regulatory pathways. Results C1QTNF6 was upregulated in stage I LUAD tissues compared with adjacent non-cancerous tissues. Concurrently, C1QTNF6 knockdown could remarkably inhibit cell proliferation, migratory and invasive abilities, while overexpression of C1QTNF6 presented opposite results. Additionally, miR‐29a-3p may serve as an upstream regulator of C1QTNF6 and reduce the expression of C1QTNF6. Subsequent experiments showed that miR‐29a-3p could decrease the cell mobility and proliferation positive cell rates, as well as reduce the migratory and invasive possibilities in LUAD cells via downregulating C1QTNF6. Moreover, RNA sequencing analysis demonstrated that the cytokine-cytokine receptor interaction pathway may participate in the process of C1QTNF6 regulating tumor progression. Conclusion Our study first demonstrated that downregulation of C1QTNF6 could inhibit tumorigenesis and progression in LUAD cells negatively regulated by miR‐29a-3p. These consequences could reinforce our awareness and understanding of the underlying mechanism and provide a promising therapeutic target for LUAD.

show abstract

Section: Discussionmentioning

confidence: 99%

C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

Lin

et al. 2022

BMC Pulm Med

View full text Add to dashboard Cite

show abstract

“…Smad nuclear interacting protein 1 (SNIP1) is a major gene that regulates cyclin D1 mRNA stability during cotranscription or posttranscription stages, and its overexpression alone is sufficient to cause tumorigenesis. 39 Increasing research has indicated that SNIP1 might be a significant prognostic predictor in patients with cervical cancer, 40 non-small cell lung cancer, 41 osteosarcoma, 42 and tongue squamous cell carcinoma. 43 The above studies suggest that SNIP1 may serve as an important prognostic marker in cancer.…”

Section: Discussionmentioning

confidence: 99%

Development and Validation of a Prognostic Model of RNA-Binding Proteins in Colon Adenocarcinoma: A Study Based on TCGA and GEO Databases

Zhu

Chen

Hou

2021

CMAR

View full text Add to dashboard Cite

Background: Previous studies reported that dysregulation of RNA-binding proteins (RBPs) is significantly associated with the development of cancer. However, there are few studies to date on the role of RBPs in colon adenocarcinoma (COAD). Methods: RNA sequencing and clinical data for COAD patients were downloaded from The Cancer Genome Atlas (TCGA) database to identify differentially expressed (DE) RBPs between COAD tissue and normal colon tissue, and then the expression and prognostic significance of these RBPs were investigated in detail by systematic bioinformatics analysis. qRT-PCR was used to validate the expressions of prognosis-related RBP-encoding genes. Results: Seven RBPs (RPL10L, ERI1, POP1, CAPRIN2, TDRD7, SNIP1 and PPARGC1A) were identified as hub genes associated with prognosis by a series of regression analyses, and were then used to construct a prognostic model. Further analysis based on this model indicated that the overall survival (OS) of the high-risk groups was lower than that of the low-risk groups. In this prognostic model, the area under the ROC curve (AUC) was 0.694, 0.709 and 0.665 for the TCGA cohort at 1, 3 and 5 years, respectively, while the AUC was 0.671, 0.633 and 0.601 for the GEO combined cohort at 1, 3 and 5 years, respectively, indicating the good predictive ability of the model. We also built a nomogram based on the 7 RBPs in the TCGA cohort, and the model showed good discriminatory ability for COAD. Conclusion:We screened seven prognosis-related genes in COAD patients based on RBPrelated genes, validated the expressions of the seven prognosis-related RBP-encoding genes by qRT-PCR and constructed a prognosis-related nomogram for patients with COAD.

show abstract

“…The up-regulation of miR-29a-3p distinctly reduced EC cells proliferation, colony formation, migration, invasion in vitro and growth in vivo. In previous researches, miR-29a-3p has been found to be acted as an important tumor suppressor in multiple human tumors [27,28]. miR-29a-3p was lower expressed in laryngocarcinoma tissues than that in control tissues.…”

Section: Discussionmentioning

confidence: 84%

“…Additionally, miR-29a-3p inhibited the proliferation, migration and invasion of gastric cancer cells [ 14 ]. In cervical cancer, miR-29a-3p attenuated the proliferation and migration of tumor cells [ 29 ]. The inhibition of miR-29a-3p expression induced epithelial-mesenchymal transition in ovarian cancer cells [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

miR-29a-3p inhibits endometrial cancer cell proliferation, migration and invasion by targeting VEGFA/CD C42/PAK1

et al. 2021

View full text Add to dashboard Cite

Background This study aimed to investigate the mechanism of miR-29a-3p in regulating endometrial cancer (EC) progression. Methods A total of 72 EC patients were enrolled. EC cells were transfected. Cells proliferation, cloning ability, migration and invasion were researched by MTT assay, colony formation experiment, cell scratch test and Transwell experiment respectively. Dual-luciferase reporter assay was performed. Xenograft experiment was conducted using nude mice. miR-29a-3p, VEGFA, CDC42, PAK1 and p-PAK1 expression in cells/tissues was investigated by qRT-PCR and Western blot. Results miR-29a-3p expression was aberrantly reduced in EC patients, which was associated with poor outcome. miR-29a-3p inhibited EC cells proliferation, cloning formation, migration and invasion (P < 0.05 or P < 0.01 or P < 0.001). miR-29a-3p inhibited CDC42/PAK1 signaling pathway activity in EC cells (P < 0.01). VEGFA expression was directly inhibited by miR-29a-3p. miR-29a-3p suppressed EC cells malignant phenotype in vitro and growth in vivo by targeting VEGFA/CDC42/PAK1 signaling pathway (P < 0.05 or P < 0.01). Conclusion miR-29a-3p inhibits EC cells proliferation, migration and invasion by targeting VEGFA/CDC42/PAK1 signaling pathway.

show abstract

miR-29a-3p directly targets Smad nuclear interacting protein 1 and inhibits the migration and proliferation of cervical cancer HeLa cells

Cited by 23 publications

References 33 publications

C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

Development and Validation of a Prognostic Model of RNA-Binding Proteins in Colon Adenocarcinoma: A Study Based on TCGA and GEO Databases

miR-29a-3p inhibits endometrial cancer cell proliferation, migration and invasion by targeting VEGFA/CD C42/PAK1

Contact Info

Product

Resources

About