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Last update 08 May 2025

MSI2

Last update 08 May 2025

Basic Info

Synonyms

MSI2, musashi RNA binding protein 2, Musashi-2

+ [1]

Introduction

RNA binding protein that regulates the expression of target mRNAs at the translation level. May play a role in the proliferation and maintenance of stem cells in the central nervous system (By similarity).

Drugs associated with MSI2

Ro 08-2750

Target

MSI2

Mechanism

MSI2 inhibitors

Active Org.

Memorial Sloan Kettering Cancer Center

Originator Org.

Tocris Cookson Ltd.

Active Indication

B-Cell Lymphoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MSI2

100 Translational Medicine associated with MSI2

0 Patents (Medical) associated with MSI2

302

Literatures (Medical) associated with MSI2

04 May 2025·International Journal of Radiation Biology

Blocking MSI2 alleviated radiation-induced pulmonary fibrosis through inhibiting epithelial-mesenchymal transition

Article

Author: Yao, Liuhuan ; Wei, Rongbing ; Liu, Tingting ; Liu, Hu ; Liu, Ruling ; Li, Bailong ; Zhao, Jianpeng ; Cai, Shanlin ; Guo, Jiaming

PURPOSEIonizing radiation (IR) has been shown to induce epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AECs), which is a critical cause of radiation-induced pulmonary fibrosis (RIPF). In this study, we investigated the role and molecular mechanisms of musashi2 (MSI2), an RNA-binding protein, in IR-induced EMT of AECs for aiming at potential therapeutic strategies to prevent RIPF.MATERIALS AND METHODSChanges in the expression levels of MSI2 and EMT markers (E-cadherin, N-cadherin, and Vimentin) induced by IR in AECs were detected by western blot (WB). Then, the effect of MSI2 on IR-induced EMT of AECs was investigated by observing morphological changes and detecting expression of MSI2 and EMT markers by WB and immunofluorescence (IF). RNA-Seq analysis, WB and RT-qPCR were used to identify the targets of MSI2.RESULTSWe observed that IR could cause a significant increase of MSI2 protein expression, a down-regulation of E-cadherin and an up-regulation of Vimentin and N-cadherin in AECs (MLE-12 and RLE-6TN cells). We also revealed that MSI2 was involved in regulating the alteration of morphology and EMT-related markers in AECs after irradiation, suggesting the occurrence of EMT regulated by MSI2. Moreover, we found the mechanism of MSI2 participating in EMT by regulating the expression of transcription factor ZEB1, acting as a downstream target of MSI2 in IR-induced EMT of AECs.CONCLUSIONSOur study unveils the critical role of MSI2 in IR-induced EMT of AECs and preliminarily elucidates its molecular mechanisms, providing new insights into the process of IR-induced pulmonary fibrosis.

01 Apr 2025·The Kaohsiung Journal of Medical Sciences

ELK4 transcription promotes MSI2‐mediated progression of non‐small cell lung cancer through the TGF‐β/SMAD3 pathway

Article

Author: Zhang, Yi‐Wei ; Shi, Guo‐Cui ; Sun, Jia‐Wei ; Liu, Cui ; Zhu, Jin‐Song ; Teng, Yu‐Qing

AbstractNon‐small cell lung cancer (NSCLC) is a primary contributor to global cancer‐related mortality. Musashi‐2 (MSI2), an RNA‐binding protein (RBP), is upregulated in specific NSCLC tumor subgroups. The current investigation evaluated the role and underlying mechanism of MSI2 in NSCLC. The expression levels of ELK4, MSI2, SMAD3, p‐SMAD3 and TGFβR1 were assessed via RT–qPCR or Western blot. Chromatin immunoprecipitation (ChIP) and dual luciferase reporter assays were used to confirm the interaction between ELK4 and MSI2. The proliferation, migration and invasion of NSCLC cells were determined via MTT, colony formation, and transwell assays, respectively. A xenograft tumor model was established in BALB/c nude mice. Immunohistochemical (IHC) staining was used to test Ki67 expression. We found that MSI2 and ELK4 expression levels were increased in NSCLC tissues and cells. ELK4 depletion suppressed the proliferation, migration and invasion of NSCLC cells. ELK4 acts as a transcription factor and promotes the transcription of MSI2. MSI2 depletion repressed NSCLC cell proliferation, migration and invasion through the TGF‐β/SMAD3 pathway. Overexpression of ELK4 reversed the inhibitory effect of MSI2 repression on NSCLC progression. These results confirmed that ELK4 is a direct regulator of MSI2 expression and that MSI2 promotes NSCLC progression through TGF‐β/SMAD3 activation, suggesting the potential clinical value of inhibiting MSI2 in NSCLC.

01 Apr 2025·Molecular Carcinogenesis

LncRNA FGD5‐AS1 Facilitates Hepatocellular Carcinoma Cell Stemness by Enhancing PKD1 mRNA Stability Through Binding With MSI2

Article

Author: Liu, Rongrong ; Zhou, Tianli ; He, Chenkun

ABSTRACTHepatocellular carcinoma (HCC) is a major global health concern that accounts for more than 80% of all primary hepatic carcinomas. The long noncoding RNA FGD5 antisense RNA 1 (FGD5‐AS1) has been linked to HCC cell stemness and proliferation. However, the exact function of FGD5‐AS1 in HCC remains unclear. Cell viability and proliferation were examined using the CCK8 and colony formation assays, respectively. Cell stemness was examined using a sphere formation assay. To investigate the relation between Musashi 2 (MSI2) and FGD5‐AS1 (or protein kinase D1 [PKD1]), RNA immunoprecipitation and RNA pull‐down assays were used. Furthermore, a xenograft mouse model was established to evaluate the function of FGD5‐AS1 in vivo. FGD5‐AS1, MSI2, and PKD1 were upregulated in the HCC tissues. FGD5‐AS1 knockdown significantly inhibited the viability, proliferation, and stemness of HCC cells and decreased the expression of MSI2, PKD1, octamer‐binding transcription factor 4, SOX2, NANOG, and Prominin‐1 in HCC cells. Mechanistically, FGD5‐AS1 increased PKD1 mRNA stability by upregulating MSI2 expression. Both MSI2 and PKD1 ameliorated sh‐FGD5‐AS1's inhibition of HCC cell viability, proliferation, and stemness. Furthermore, FGD5‐AS1 silencing inhibited HCC tumor growth and stemness in vivo. FGD5‐AS1 promotes the stemness of HCC cells by activating the MSI2/PKD1 axis. Our study provides a new theoretical foundation for the development of novel HCC treatments.

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MSI2

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