Knockdown of MSI1 inhibits the proliferation of human oral squamous cell carcinoma by inactivating STAT3 signaling

Wang, Chen‐Fei; Zhang, Hong‐Chuang; Feng, Xinmei; Song, Xiaomeng; Wu, Yunong

doi:10.3892/ijmm.2019.4181

Cited by 14 publications

(13 citation statements)

References 32 publications

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“…The enhancement of Numb followed by MSI1 knockdown inhibits intracellular processing of Notch. On the other way, MSI1 silencing in oral squamous cell carcinoma cell lines represses cell proliferation and progression through inactivation of the STAT3 signaling pathway [42]. Reduction of MSI1 expression in breast cancer cell lines decreased the NOTCH1, c-MYC, ERBB2, and ERK1/2 expressions, which eventually inhibited the survival of tumor cells [26].…”

Section: Association Of Msi1 Expression and Cancersmentioning

confidence: 99%

Intracellular functions of RNA-binding protein, Musashi1, in stem and cancer cells

et al. 2020

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RNA-binding protein, musashi1 (MSI1), is a main protein in asymmetric cell division of the sensory organ precursor cells, whereas its expression is reported to be upregulated in cancers. This protein is a critical element in proliferation of stem and cancer stem cells, which acts through Wnt and Notch signaling pathways. Moreover, MSI1 modulates malignancy and chemoresistance of lung cancer cells via activating the Akt signaling. Due to the main role of MSI1 in metastasis and cancer development, MSI1 would be an appropriate candidate for cancer therapy. Downregulation of MSI1 inhibits proliferation of cancer stem cells and reduces the growth of solid tumors in several cancers. On the other hand, MSI1 expression is regulated by microRNAs in such a way that several different tumor suppressor miRNAs negatively regulate oncogenic MSI1 and inhibit migration and tumor metastasis. The aim of this review is summarizing the role of MSI1 in stem cell proliferation and cancer promotion.

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Section: Association Of Msi1 Expression and Cancersmentioning

confidence: 99%

Intracellular functions of RNA-binding protein, Musashi1, in stem and cancer cells

et al. 2020

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“…16 It activates the STAT3 signaling to facilitate the progression of oral squamous cell carcinoma. 17 In glioma, MSI1 up-regulates intercellular adhesion molecule-1, down-regulates Tensin3, and activates PKR/eIF2α signaling and IL-6/Akt signaling to mediate the migration and invasion of glioma cells, and its overexpression is linked to the chemoresistance and radioresistance of glioma cells. 21,[42][43][44][45] However, there are few researches focusing on the mechanism of MSI1 dysregulation in glioma.…”

Section: Dovepressmentioning

confidence: 99%

“…16 MSI1 is highly expressed in many cancers, whose role is to facilitate tumor cell growth and suppress apoptosis. [17][18][19] Previous researches validate that the expression of MSI1 in medulloblastoma tissue is higher than that in normal brain tissues, and its high expression is also related to the poor prognosis of glioma and medulloblastoma. [20][21][22][23] These findings suggest that MSI1 promotes tumorigenesis and progression of gliomas.…”

Section: Introductionmentioning

confidence: 98%

<p>LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma</p>

Zhu¹,

Liu²,

Liu³

et al. 2020

CMAR

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Background: This study aims at probing into the expression, function, and mechanism of LINC01094 and miR-330-3p in glioma. Materials and Methods: qRT-PCR was employed to examine LINC01094 and miR-330-3p expressions in gliomas. After gain-of-function and loss-of-function models were constructed, CCK-8 and Transwell assays were used to detect the proliferation, migration and invasion of LN229 and U251 cells, respectively. Additionally, dual luciferase reporter gene assay was utilized to verify the binding site between m4iR-330-3p and LINC01094, miR-330-3p, and the 3ʹUTR of musashi RNA binding protein 1 (MSI1). Then, RNA pull-down, RIP, qRT-PCR and Western blot were employed to detect the regulatory relationships among LINC01094, miR-330-3p, and MSI1. Results: The expression of LINC01094 was elevated in glioma tissues and cell lines, and the high expression of LINC01094 was associated with high grade of glioma. In contrast, miR-330-3p was lowly expressed in glioma tissue. Overexpression of LINC01094 or downregulation of miR-330-3p promoted the proliferation, migration, and invasion of glioma cells, while LINC01094 knockdown or miR-330-3p up-regulation impeded these processes. miR-330-3p was identified as a target miRNA of LINC01094, and it could be negatively regulated by LINC01094. In addition, miR-330-3p antagonized the function of LINC01094 by negatively regulating MSI1. Conclusion: LINC01094 promotes the proliferation, migration, and invasion of glioma cells by adsorbing miR-330-3p and up-regulating the expression of MSI1.

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“…MSI1 increases proliferation of mammary stem cells through triggering of two signaling pathways; Notch and Wnt [4]. Moreover, MSI1 is strongly expressed in multiple solid tumors such as brain [5][6][7], lung [8], ovary, squamous oral, colorectal and renal cancers [9][10][11][12]. On the other hand, MSI2 is reported to be upregulated in hematopoietic cancer cells [13].…”

Section: Introductionmentioning

confidence: 99%

Increased expression of MUSASHI1 in epithelial breast cancer cells is due to down regulation of miR-125b

Forouzanfar

Lachinani

Dormiani

et al. 2021

BMC Mol and Cell Biol

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Background Musashi1 (MSI1) is an oncogenic protein with a crucial role in the proliferation and characteristics of the epithelial cells in breast cancer. The change in expression of MSI1 has a role in solid tumor progression. There are different factors that regulate MSI1 expression in various cancer tissues including microRNAs which are considered as one of the most important of these factors. The aim of our study is identification of the molecular cause of maximal expression of MSI1 in epithelial breast cancer cell lines. Results Among predicted microRNAs, miR-125b, miR-637 and miR-802 were able to significantly reduce the luciferase activity. In addition, the relative expression of these three miRNAs were measured in the cancerous cell lines that results showed a significant reduction in expression of all microRNAs. On the other hand, only the overexpression of miR-125b caused a change in the expression pattern of MSI1 in breast epithelial cancer cell lines. Accordingly, our results demonstrated that the exogenous expression of miR-125b decreased not only the MSI1 protein but also expression of epithelial markers in breast cancer cells. Conclusions The results of luciferase reporter assay showed that MSI1 is a direct target for miR-125b in epithelial breast cancer cells. Moreover, higher amount of MSI1 in those cell lines seems due to the reduced amount of miR-125b, which is responsible for epithelial features of those kinds of cancer cells. Therefore, the modulation of miR-125b may be a potential approach to help to combat against epithelial breast tumors.

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Knockdown of MSI1 inhibits the proliferation of human oral squamous cell carcinoma by inactivating STAT3 signaling

Cited by 14 publications

References 32 publications

Intracellular functions of RNA-binding protein, Musashi1, in stem and cancer cells

Intracellular functions of RNA-binding protein, Musashi1, in stem and cancer cells

<p>LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma</p>

Increased expression of MUSASHI1 in epithelial breast cancer cells is due to down regulation of miR-125b

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