Molecular Characterization of the MicroRNA-138-Fos-like Antigen 1 (FOSL1) Regulatory Module in Squamous Cell Carcinoma

Jin, Y.; Wang, Cheng; Liu, Xiqiang; Mu, Wenbo; Chen, Zujian; Yu, Dongsheng; Wang, Anxun; Dai, Yang; Zhou, Xiaofeng

doi:10.1074/jbc.c111.296707

Cited by 49 publications

(57 citation statements)

References 31 publications

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“…Our results indicated that overexpression of miR-138 could inhibit cell growth and colony formation in NPC cells in vitro and tumorigenesis in vivo, and, moreover, the effects were reversed when the endogenous miR-138 was inhibited. These consistent results suggest that miRNA-138 could be a tumor suppressor in NPC, which is consistent with previous reports that miR-138 functions as a tumor suppressor through its anti-metastatic and anti-apoptotic effects in a variety of tumors, including squamous cell carcinoma, 24 clear cell renal cell carcinoma, 25 tongue squamous cell carcinoma 26 and head and neck squamous cell carcinoma. 27 Further investigations revealed that CCND1 is a target of miR-138 for the first time.…”

Section: 16supporting

confidence: 81%

MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene

Liu

Lv²,

Wang³

et al. 2012

Cell Cycle

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Section: 16supporting

confidence: 81%

MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene

Liu

Lv²,

Wang³

et al. 2012

Cell Cycle

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“…miR-138 has been found to be downregulated in multiple human cancers, and downregulation of miR-138 contributes to cancer cell proliferation and invasion and inhibits apoptosis via different mechanisms (33)(34)(35)(36)(37)(38)(39)(40). However, the expression of miR-138 has also been shown to be upregulated in tumor-initiating glioma stem cells (GSC) compared with nonneoplastic tissues, and upregulation of miR-138 is associated with tumor recurrence and survival (41).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

Gong

Song

Lin

et al. 2013

Clinical Cancer Research

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Purpose: Constitutive activation of NF-kB signaling plays vital roles in esophageal squamous cell carcinoma (ESCC) progression. The aim of this study was to evaluate the effect of miR-138 on NF-kB activation and ESCC progression.Experimental Design: Expression of miR-138 in ESCC cell lines, ESCC tissues, and 205 archived ESSC specimens was determined using real-time PCR analysis. Anchorage-independent growth, chicken chorioallantoic membrane, Transwell matrix invasion and Annexin V-binding assays, and a xenograft tumor model were used to determine the role of miR-138 in ESCC progression. The effect of miR-138 on NF-kB activation was investigated using IKK in vitro kinase, electrophoretic mobility shift, lipid raft isolation, and luciferase reporter assays.Results: miR-138 was downregulated and inversely correlated with tumor progression and patient survival in ESCCs. Downregulation of miR-138 enhanced, whereas upregulation of miR-138 reduced, the aggressive phenotype of ESCC cells both in vitro and in vivo. Silencing miR-138 promoted K63-linked polyubiquitination of the NF-kB signaling intermediaries TRAF2 and RIP1 and sustained NF-kB activation. Furthermore, downregulation of miR-138 induced lipid raft formation via upregulating multiple components of lipid rafts, including FLOT1, FLOT2, and caveolin-1. Importantly, the in vitro analysis was consistent with a significant inverse correlation between miR-138 expression and NF-kB hyperactivation in a cohort of human ESCC specimens.Conclusion: Our results show that miR-138 functions as a tumor-suppressive miRNA and that downregulation of miR-138 contributes to constitutive NF-kB activation and ESCC progression.

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“…Treatment of xenograft mouse models with miR-192-DOPC (1,2-dioleoyl-sn-glycero-3-phosphocholine) leads to inhibition of angiogenesis and tumor growth (67). MiR-551b-3p is located in a genomic region frequently amplified in high-grade serous EOC (68). MiR-551b-3p overexpression in high-grade EOC is associated with decreased overall survival.…”

Section: Microrna Molecules As Therapy For Eocmentioning

confidence: 99%

The role of MicroRNA molecules and MicroRNA-regulating machinery in the pathogenesis and progression of epithelial ovarian cancer

Wang

Ivan

Hawkins

2017

Gynecologic Oncology

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MicroRNA molecules are small, single-stranded RNA molecules that function to regulate networks of genes. They play important roles in normal female reproductive tract biology, as well as in the pathogenesis and progression of epithelial ovarian cancer. DROSHA, DICER, and Argonaute proteins are components of the microRNA-regulatory machinery and mediate microRNA production and function. This review discusses aberrant expression of microRNA molecules and microRNA-regulating machinery associated with clinical features of epithelial ovarian cancer. Understanding the regulation of microRNA molecule production and function may facilitate the development of novel diagnostic and therapeutic strategies to improve the prognosis of women with epithelial ovarian cancer. Additionally, understanding microRNA molecules and microRNA-regulatory machinery associations with clinical features may influence prevention and early detection efforts.

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Molecular Characterization of the MicroRNA-138-Fos-like Antigen 1 (FOSL1) Regulatory Module in Squamous Cell Carcinoma

Cited by 49 publications

References 31 publications

MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene

MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

The role of MicroRNA molecules and MicroRNA-regulating machinery in the pathogenesis and progression of epithelial ovarian cancer

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