miR-217 inhibits the migration and invasion of HeLa cells through modulating MAPK1

Zhu, Lihong; Yang, Sheng; Wang, Jianfeng

doi:10.3892/ijmm.2019.4328

Cited by 22 publications

(20 citation statements)

References 40 publications

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“…These kinases are involved in genomic stability, DNA damage, cell cycle progression, and epithelial-mesenchymal transition (47)(48)(49)(50)(51). Moreover, these kinases affect tumor development and progression by regulating tumor cell migration, invasion, and apoptosis (52,53). In RCC, differentially expressed CXC chemokines may modulate genomic stability, DNA repair, cell cycle progression, and the epithelial-mesenchymal transition by regulating these kinases.…”

Section: Discussionmentioning

confidence: 99%

Identification of Therapeutic Targets and Prognostic Biomarkers Among CXC Chemokines in the Renal Cell Carcinoma Microenvironment

Zeng¹,

Sun

Li³

et al. 2020

Front. Oncol.

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Background: Renal cell carcinoma (RCC) is one of the most common malignances with an ever-increasing incidence and high mortality. Cross-talk between cancer cells and interstitial cells exerts significant effects on neoplasia and tumor development and is modulated in part by chemokines. CXC chemokines in the tumor microenvironment can modulate immune cell trafficking and regulate tumor cell activities, thus exerting anti-tumor immunological effects and affecting patient outcomes; however, the expression and prognostic values of CXC chemokines in RCC have not been clarified. Methods: ONCOMINE, GEPIA, UALCAN, cBioPortal, GeneMANIA, DAVID 6.8, Metascape, TRRUST, LinkedOmics, and TIMER were utilized in this study. Results: The transcriptional levels of CXCL1/2/5/6/9/10/11/16 in RCC tissues were significantly elevated while the transcriptional levels of CXCL3/7/12/13 were significantly reduced. A significant correlation was found between the expression of CXC1/5/9/10/11/13 and the pathological stage of RCC patients. RCC patients with low transcriptional levels of CXCL1/2/3/5/13 were associated with a significantly better prognosis. The functions of differentially expressed CXC chemokines are primarily related to the chemokine signaling pathway, cytokine-cytokine receptor interactions, and the ILK signaling pathway. Our data suggest that RELA, NFKB1, and SP1 are key transcription factors for CXC chemokines, and the SRC family of tyrosine kinases (LCK, LYN, and FYN), mitogen-activated protein kinases (MAPK1 and MAPK3), and CSNK1D are CXC chemokine targets. We found significant correlations among the expression of CXC chemokines and the infiltration of six types of immune cells (B cells, CD8 + T cells, CD4 + T cells, macrophages, neutrophils, and dendritic cells). Conclusions: Our results may provide novel insights for the selection of immunotherapeutic targets and prognostic biomarkers for renal cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Identification of Therapeutic Targets and Prognostic Biomarkers Among CXC Chemokines in the Renal Cell Carcinoma Microenvironment

Zeng¹,

Sun

Li³

et al. 2020

Front. Oncol.

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“…miR-217 has been reported to have antitumor effects in multiple types of cancer ( 34 , 35 ). For example, miR-217 inhibits EMT transition by targeting PTPN14 in gastric carcinoma ( 36 ) and suppresses HeLa cell migration and invasion by regulating MAPK1 ( 37 ). The current study validated the binding between LINC00467 and miR-217, as well as their negative correlation in OS.…”

Section: Discussionmentioning

confidence: 99%

LINC00467 facilitates osteosarcoma progression by sponging miR‑217 to regulate KPNA4 expression

et al. 2021

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Osteosarcoma (OS) is a musculoskeletal malignancy that originates from interstitial cells. An increasing number of studies have verified that long non-coding RNAs (lncRNAs) participate in the progression of numerous types of cancer. It has been reported that LINC00467 is a cancer-promoting gene in some types of cancer; however, the regulatory mechanism of LINC00467 in OS remains unknown. In the present study, reverse transcription-quantitative PCR was used to determine LINC00467 expression in OS tissues and cells. Additionally, the impact of LINC00467-knockdown on OS cell proliferation, migration and invasion was analyzed using Cell Counting Kit-8, colony formation and Transwell assays, as well as western blot analysis. RNA pulldown and luciferase reporter assays were conducted to investigate the regulatory mechanism of LINC00467 in OS. The results delineated that LINC00467 expression was elevated in OS tissues and cells, and that high LINC00467 expression was associated with a poor prognosis in patients with OS. LINC00467 inhibition suppressed OS progression by inhibiting cell proliferation, migration, invasion and epithelial-mesenchymal transition. LINC00467 served as a molecular sponge for microRNA (miR)-217, while karyopherin subunit α4 (KPNA4) was a downstream target gene of miR-217. Moreover, the overexpression of KPNA4 reversed the inhibitory effects of LINC00467 inhibition on OS progression. Therefore, the present study elucidated the potential mechanism of LINC00467 in OS and indicated that LINC00467 exerted its carcinogenic effects on OS through the miR-217/KPNA4 axis, implying that LINC00467 may be a novel potential therapeutic target for OS.

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“…MiR-217 inhibits MAPK1 and reduces cell viability, migration, and invasion while enhancing cell apoptosis. They have introduced miR-217 as a tumor suppressor gene in cervical cancer [27]. Another study found that miR-217 expression was different in normal pancreatic cells compared with pancreatic cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of valproic acid on miRNAs affecting histone deacetylase in a model of anaplastic thyroid cancer

et al. 2021

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Thyroid cancer is the most common malignant tumor of the endocrine system seen in the thyroid gland.More than 90% of thyroid cancers comprise papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC). Although anaplastic thyroid carcinoma (ATC) accounts for less than 2% of thyroid cancer. But patients' lifespan after diagnosis is about 6 months. Surgical interventions, radioactive iodine use, and chemotherapy are not su cient in the treatment of ATC, so alternative therapies are needed. The WST-1 assay test was performed to evaluate the anti-proliferative effects of Valproic acid (VPA). Also, Effect of VPA on miRNAs affecting histone deacetylase were determined by Quantitative RT-PCR. In BRAFV600E / mut SW1736 (SW1736) cell line IC50 dose for VPA found 1.6 mg/ml. in our study, the level of oncogenic genes expression in cells treated with VPA, including miR-184, miR-222-5p, miR-124-3p, and miR-328-3p, decreased. Also, the expression of tumor inhibitory genes is miR- 323-5p, miR-182-5p, miR-138-5p, miR-217, miR-15a-5p, miR-29b-3p, miR-324-5p and miR-101-5p increased signi cantly. VPA can ad-just countless gene expression patterns, including microRNAs (miRNAs), by targeting histone deacetylase (HDAC). We got very promising results with VPA.

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miR-217 inhibits the migration and invasion of HeLa cells through modulating MAPK1

Cited by 22 publications

References 40 publications

Identification of Therapeutic Targets and Prognostic Biomarkers Among CXC Chemokines in the Renal Cell Carcinoma Microenvironment

Identification of Therapeutic Targets and Prognostic Biomarkers Among CXC Chemokines in the Renal Cell Carcinoma Microenvironment

LINC00467 facilitates osteosarcoma progression by sponging miR‑217 to regulate KPNA4 expression

Effect of valproic acid on miRNAs affecting histone deacetylase in a model of anaplastic thyroid cancer

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