MiR-144 suppresses proliferation, invasion, and migration of breast cancer cells through inhibiting CEP55

Yin, Yong; Cai, Jingjing; Meng, Fandong; Sui, Chengguang; Jiang, Youyu

doi:10.1080/15384047.2017.1416934

Cited by 48 publications

(40 citation statements)

References 30 publications

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“…Moreover, miR-144-3p induced cell cycle arrest and apoptosis in human pancreatic cancer cells (PANC-1 cells) . It is reported that, miR-144 could suppress proliferation, induce cell cycle arrest and cell apoptosis by targeting CEP55 human breast cancer cell lines MCF-7, MDA-MB-231 and SK-BR-3 (Yin et al, 2018). Our results showed that, suppression of miR-144-3p can inhibit mitochondrial apoptosis via downregulation of Bax and upregulation of Bcl-2 and decreasing caspase-3 in human ovarian cancer cells OVCAR-3 and SKOV-3.…”

Section: Discussionsupporting

confidence: 50%

Suppression of MicroRNA-144 Promotes CXCR4 and CXCL12 Expression and Downregulates Apoptosis in Ovarian Cancer Cells

Turut

Acıdereli

Çevik

2020

Preprint

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MicroRNAs are important regulators in the growth and metastasis of ovarian cancers. Many assays were established to identify the role of miR-144-3p in ovarian cancer cells and its interaction with COX-2 and chemokines (CXCR4 and CXCL12). The ovarian cancer cells (OVCAR-3 and SKOV-3) were transfected with Anti-miR-144 to downregulate the miR-144-3p and cultured for 36 h. We herein examined the cell viability, colony formation, cell migration, COX-2 reporter activity, the protein expressions of CXCR4, CXCL12, COX-2, VEGF, Caspase-3, BAX and Bcl-2. We have observed that the suppression of miR-144-3p significantly increased the cell proliferation and migration and decreased the apoptosis. Moreover, the downregulation of miR-144-3p markedly increased the COX-2, CXCR4, CXCL12 and VEGF expression in OVCAR-3 and SKOV-3 ovarian cancer cells. In conclusion, miR-144-3p may play important roles in the regulation of chemokine receptor CXCR4 and its ligand CXCL12 in the progressive ovarian tumors expressing COX2. These data suggests that miR-144 has the novel therapeutic targets for the cancer therapy and cancer prevention.

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Section: Discussionsupporting

confidence: 50%

Suppression of MicroRNA-144 Promotes CXCR4 and CXCL12 Expression and Downregulates Apoptosis in Ovarian Cancer Cells

Turut

Acıdereli

Çevik

2020

Preprint

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“…Additionally, this study showed that the expression of miR-144 can repress the process of EMT in MCF-7 and MDA-MB-231 cell lines [146]. MiR-144 via the downregulation of CEP55 could inhibit proliferation, invasion, migration, and arresting cell cycle and accelerating apoptosis of breast cancer cells [147]. Another study by Yu L et al found that miR-144 might function as an oncomiR by an increase in the survival rate of breast cancer cells.…”

Section: Mir-144 In Breast Cancermentioning

confidence: 74%

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Kooshkaki

Rezaei

Rahmati

et al. 2020

IJMS

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MicroRNAs (miRNAs) are small and non-coding RNAs that display aberrant expression in the tissue and plasma of cancer patients when tested in comparison to healthy individuals. In past decades, research data proposed that miRNAs could be diagnostic and prognostic biomarkers in cancer patients. It has been confirmed that miRNAs can act either as oncogenes by silencing tumor inhibitors or as tumor suppressors by targeting oncoproteins. MiR-144s are located in the chromosomal region 17q11.2, which is subject to significant damage in many types of cancers. In this review, we assess the involvement of miR-144s in several cancer types by illustrating the possible target genes that are related to each cancer, and we also briefly describe the clinical applications of miR-144s as a diagnostic and prognostic tool in cancers.Int. J. Mol. Sci. 2020, 21, 2578 2 of 23 of a mRNA molecule [3]. MiRNAs indicate a new perspective in the study of cancers. More than 50% of miRNA genes were discovered to be located within the genomic regions that are involved in cancers, suggesting their role in human cancer pathogenesis. In pathological conditions, MiRNAs can negatively regulate gene expression and they are associated with tumor growth, apoptosis, invasion, and metastasis. In the past, several studies have indicated the ability of miRNAs in the inhibition of tumors as a critical option for the improvement of cancer therapy [4,5]. Tumor activator miRNAs, called oncomiRs, are overexpressed in various cancers. On the contrary, suppressive tumor miRNAs are underexpressed [6][7][8]. Among several miRNAs assessed, miR-144s seem to have a role in several cancers. These miRNAs are located in the chromosomal region 17q11.2, being significantly destroyed in many types of cancers. The predicted stem-loop structure of miR-144s recognized by the miRBase (http://mirbase.org/) is shown in Figure 1A. The miR-144 hairpin gives rise to the "guide strand" miR-144-5p and the sister "passenger" strand miR-144-3p ( Figure 1B).

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“…Recent years, the expression status and biological function of miR-144-3p have been intensively investigated in many cancers [9,[20][21][22]. However, previous studies have produced inconsistent results.…”

Section: Discussionmentioning

confidence: 99%

“…International Publisher including breast cancer, glioblastoma, hepatocellular carcinoma, and et al [9][10][11]. However, the biological role and clinical significance of miR-144-3p in OSCC are still not known.…”

Section: Ivyspringmentioning

confidence: 99%

MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

Jiang

et al. 2020

J. Cancer

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An increasing number of studies indicate that miR-144-3p is dysregulated in numerous cancers, but its role in oral squamous cell carcinoma (OSCC) remains largely unknown. Herein we demonstrated that miR-144-3p expression was significantly downregulated in OSCC tissues and cell lines. Moreover, the low level of miR-144-3p expression was associated with the clinical characteristics of OSCC patients. Furthermore, ectopic expression of miR-144-3p inhibited the proliferation, migration, and invasion of OSCC cells in vitro, and blunted the tumorigenic ability of OSCC cells in vivo. Additionally, the levels of miR-144-3p were negatively correlated with the expression status of endoplasmic reticulum oxidoreduction-1-like (ERO1L) in OSCC cell lines. Subsequently, we identified that ERO1L was a direct target of miR-144-3p. Intriguingly, we found that miR-144-3p downregulation of ERO1L inhibited the activity of signal transducer and activator of transcription 3 (STAT3) in OSCC cells. Therefore, miR-144-3p suppresses tumorigenesis by targeting ERO1L/STAT3 signaling pathway in OSCC. miR-144-3p may a candidate target for OSCC treatment.

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MiR-144 suppresses proliferation, invasion, and migration of breast cancer cells through inhibiting CEP55

Abstract: MiR-144 suppressed cell proliferation, migration, invasion and induced cell cycle arrest and cell apoptosis by repressing CEP55. This might provide a promising therapy for clinical treatment.

Cited by 48 publications

References 30 publications

Suppression of MicroRNA-144 Promotes CXCR4 and CXCL12 Expression and Downregulates Apoptosis in Ovarian Cancer Cells

Suppression of MicroRNA-144 Promotes CXCR4 and CXCL12 Expression and Downregulates Apoptosis in Ovarian Cancer Cells

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

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