MicroRNA‐143/Musashi‐2/<scp>KRAS</scp> cascade contributes positively to carcinogenesis in human bladder cancer

Tsujino, Takeshi; Sugito, Nobuhiko; Taniguchi, Kohei; Honda, Ryo; Komura, Kazumasa; Yoshikawa, Yuki; Takai, Tomoaki; Minami, Koichiro; Kuranaga, Yuki; Shinohara, Haruka; Tokumaru, Yoshihisa; Heishima, Kazuki; Inamoto, Teruo; Azuma, Haruhito; Akao, Yukihiro

doi:10.1111/cas.14035

Cited by 25 publications

(19 citation statements)

References 53 publications

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“…Consistent with our results, miR-143 could target and down-regulate the expression of MSI2 in cervical cancer [18]. Similarly, Tsujino et al indicated that miR-143 could down-regulate MSI2 expression and repress bladder cancer cell proliferation through inhibition of MSI2 expression [22]. Furthermore, Fos-related antigen 2 (FOSL2) was targeted by miR-143-3p in osteosarcoma (OS), thus suppressing OS cell proliferation, migration and invasion [40].…”

Section: Discussionsupporting

confidence: 88%

“…We therefore considered that miR-143-3p was extremely critical, and through the GEO database, significantly low expression of miR-143-3p was identified in TC (Figure 1C). It has been shown that synthetic miR-143 negatively regulated MSI2 in human bladder cancer cell lines [22], and miR-143-3p could be adopted as a potential diagnostic and biomarker of TC. LINC01296 was associated with colorectal cancer [23], ESCC [24] and breast cancer [25], but the regulatory mechanism of LINC01296 in TC is still unknown.…”

Section: Resultsmentioning

confidence: 99%

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Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer

Wang

Liu

2019

Bioscience Reports

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Thyroid cancer (TC) is an endocrine malignancy with rising incidence. Long non-coding RNAs (lncRNAs) can serve as diagnostic and prognostic biomarkers for TC. Thus, we studied roles of LINC01296 in TC progression. Initially, the Gene Expression Omnibus (GEO) database was used to detect the differentially expressed genes in human TC samples and the potential mechanism. Expression of LINC01296 and miR-143-3p in TC tissues and cells was measured. The transfection of TC cells was conducted with si-LINC01296, si-Musashi 2 (MSI2), mimic or inhibitor of miR-143-3p to determine their effects on TC cell proliferation, migration, invasion, apoptosis and the AKT/STAT3 signaling pathway. Finally, in vivo assay was performed to verify role of miR-143-3p in tumorigenesis of TC cells in nude mice. LINC01296 was predicted to bind to miR-143-3p to modulate MSI2 expression, thus regulating the occurrence and development of TC. LINC01296 was up-regulated, while miR-143-3p was down-regulated in TC cells and tissues. LNC01296 specifically bound to miR-143-3p and MSI2 was a target of miR-143-3p. Besides, LINC01296 silencing or miR-143-3p overexpression inhibited migration, invasion, proliferation and advanced apoptosis of TC cells. Additionally, silenced LINC01296 or overexpressed miR-143-3p reduced phosphorylated STAT3/STAT3, phosphorylated AKT/AKT, B-cell lymphoma-2 (Bcl-2) and CyclinD1 levels but elevated BCL2-associated X (Bax), Cleaved Caspase3 and Caspase3 levels. Also, tumorigenesis of TC cells in nude mice was inhibited with the silencing of LINC01296. In summary, LINC01296/miR-143-3p/MSI2 axis regulated development of TC through the AKT/STAT3 signaling pathway.

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Section: Discussionsupporting

confidence: 88%

Section: Resultsmentioning

confidence: 99%

Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer

Wang

Liu

2019

Bioscience Reports

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“…Noguchi et al demonstrated the combination therapy with the ectopic expression of MIR143 and MIR145 showed the synergistic inhibition of bladder cancer cells through modulating PI3K/AKT and MAPK signaling pathways 11 . Recently, we discovered that MIR143‐3p negatively regulated the KRAS/Musashi‐2 cascade and, consequently, suppressed the cell growth in bladder cancer through downregulation of the KRAS protein expression level at the translational step 55 . Xu et al 56 demonstrated that MIR143 overexpression inhibits KRAS expression and its effector MAPK/ERK signaling pathway, which results in enhanced chemosensitivity to docetaxel in prostate cancer.…”

Section: The Role Of Mir143‐3p On Rat Sarcoma Signaling Network In Vmentioning

confidence: 99%

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

et al. 2020

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This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. AbstractRat sarcoma (RAS) is a well-known oncogene that plays important roles in cancer proliferation, cell survival and cell invasion. RAS exists as three major isoforms, Kirsten rat sarcoma (KRAS), Harvey rat sarcoma (HRAS) and neuroblastoma rat sarcoma (NRAS). Mutations of these genes account for approximately 30% of all cancers.Among them, KRAS mutations are the most common, responsible for 85%, followed by NRAS (12%) and HRAS (3%). Although the development of RAS inhibitors has been explored for over the past decade, so far, no effective inhibitor has been found.MicroRNA (miRNA) are a class of small non-coding RNA that control the gene expression of pleural target genes at the post-transcriptional level. MiRNA play critical roles in the physiological and pathological processes at work in cancers, such as cell proliferation, cell death, cell invasion and metastasis. MicroRNA-143 (MIR143) is known to function as a tumor suppressor in a variety of cancers. One of its known mechanisms is suppression of RAS expression and its effector signaling pathways, such as PI3K/AKT and MAPK/ERK. Within the last five years, we developed a potent chemically modified MIR143-3p that enabled us to elucidate the details of the KRAS signaling networks at play in colon and other cancer cells. In this review, we will discuss the role of MIR143-3p in those RAS signaling networks that are related to various biological processes of cancer cells. In addition, we will discuss the possibility of the use of MIR143 as a therapeutic drug for targeting RAS signaling networks. K E Y W O R D S AKT, ERK, KRAS positive circuit, MAPK, MIR143, PI3K, RAS | 1077 TOKUMARU eT Al.

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“…Musashi has two N‐terminal RNA recognition motifs (RRM), RRM1 and RRM2, that mediate the binding to motifs located at the 3′‐UTR of target mRNA . MSI2 has been reported to act as a potent cooperative oncoprotein in hematopoietic malignancies and a variety of solid tumors …”

Section: Introductionmentioning

confidence: 99%

RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression

et al. 2020

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractThe androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18-24 months of AR blocking therapy, patients invariably progress to castration-resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key molecules that interact with AR as novel strategies to treat prostate cancer and even CRPC is desperately needed. In the current study, we focused on the regulation of RNA-binding proteins (RBPs) associated with AR and determined that the mRNA and protein levels of AR were highly correlated with Musashi2 (MSI2) levels. MSI2 was upregulated in prostate cancer specimens and significantly correlated with advanced tumor grades. Downregulation of MSI2 in both androgen sensitive and insensitive prostate cancer cells inhibited tumor formation in vivo and decreased cell growth in vitro, which could be reversed by AR overexpression. Mechanistically, MSI2 directly bound to the 3′-untranslated region (UTR) of AR mRNA to increase its stability and, thus, enhanced its transcriptional activity. Our findings illustrate a previously unknown regulatory mechanism in prostate cancer cell proliferation regulated by the MSI2-AR axis and provide novel evidence towards a strategy against prostate cancer. K E Y W O R D Sandrogen receptor, mRNA stability, Musashi2, novel anti-androgen therapy, prostate cancer

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MicroRNA‐143/Musashi‐2/KRAS cascade contributes positively to carcinogenesis in human bladder cancer

Cited by 25 publications

References 53 publications

Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer

Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression

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