MALAT1 promotes the proliferation and invasion of thyroid cancer cells via regulating the expression of IQGAP1

Huang, Jiankang; Ma, Ling; Song, Wen-hua; Lu, Binfeng; Huang, Yubin; Dong, Hui-Ming; Ma, Xiang; Zhu, Zhou; Zhou, Rui

doi:10.1016/j.biopha.2016.05.039

Cited by 64 publications

(52 citation statements)

References 28 publications

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“…Thus the role of lncRNAs in the regulation of ATCs has not been analyzed. The recent study of Huang et al (24) on thyroid carcinoma cell lines suggested that FC cell line FTC133 expressed higher levels of MALAT1 compared to the SW1736 ATC cell line. Since our studies showed that PTC tumors had higher levels of MALAT1 compared to FCs and ATCs, the molecular mechanisms regulating differences in MALAT1 expression in these various thyroid tumor types must await further studies.…”

Section: Discussionmentioning

confidence: 98%

MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR

et al. 2016

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Long noncoding RNAs (lncRNAs) are important for transcription and for epigenetic or posttranscriptional regulation of gene expression, and may contribute to carcinogenesis. MALAT1 (Metastasis Associated Lung Adenocarcinoma Transcript 1), a lncRNA involved in the regulation of the cell cycle, cell proliferation and cell migration, is known to be deregulated in multiple cancers. Here we analyzed the expression of MALAT1 on 195 cases of benign and malignant thyroid neoplasms by using tissue microarrays for RNA in-situ hybridization (ISH) and real-time PCR. MALAT1 is highly expressed in normal thyroid tissues (NT) and thyroid tumors, with increased expression during progression from NT to papillary thyroid carcinomas (PTCs), but is downregulated in poorly differentiated thyroid cancers (PDCs) and anaplastic thyroid cancers (ATCs) compared to NT. Induction of epithelial to mesenchymal transition (EMT) by TGF beta in a PTC cell line (TPC1) led to increased MALAT1 expression, supporting a role for MALAT1 in EMT in thyroid tumors. This is the first ISH study of MALAT1 expression in thyroid tissues. It also provides the first piece of evidence suggesting MALAT1 downregulation in certain thyroid malignancies. Our findings support the notion that ATCs may be molecularly distinct from low grade thyroid malignancies, and suggest that MALAT1 may function both as an oncogene and as a tumor suppressor in different types of thyroid tumors.

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Section: Discussionmentioning

confidence: 98%

MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR

et al. 2016

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“…Si-MALAT1 significantly decreased the level of acetyl-H4 histone in the IQGAP1 promoter. Therefore, MALAT1 could promote the proliferation and invasion of thyroid cancer cells via regulating the expression of IQGAP1 (Huang, Ma et al, 2016).…”

Section: Malat1 Mediates Epigenetic Changesmentioning

confidence: 99%

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Chen

Huang

et al. 2018

Journal Cellular Physiology

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial-mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA-protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.

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“…For example, lncRNA MALAT1 expression is upregulated in thyroid cancer, and promotes cell proliferation and invasion through regulating the expression of IQGAP1 17. Liu et al reported that the expression of H19 is much higher in thyroid cancer tissues and cells, and over‐expressed H19 promotes cell growth, migration, and invasion via acting as a competitive endogenous RNA (ceRNA) for miR‐17‐5p and antagonizing the repression of miR‐17‐5p on its target YES1 18.…”

Section: Introductionmentioning

confidence: 99%

Identification of differential expressed lncRNAs in human thyroid cancer by a genome‐wide analyses

et al. 2018

Cancer Medicine

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Recently, a growing number of evidence has revealed that long noncoding RNAs (lncRNAs) act as key regulators in various cellular biologic processes, and dysregulation of lncRNAs involves in tumorigenesis and cancer progression. However, the expression pattern, clinical relevance, and biologic function of most lncRNAs in human thyroid cancer remain unclear. To identify more thyroid‐cancer‐associated lncRNAs, we analyzed the expression profile of lncRNAs in thyroid cancer tissues and adjacent normal or non‐tumor tissues using RNA sequencing data and gene microarray data from The Cancer Genome Atlas and Gene Expression Omnibus. Annotation and analyses of these data revealed that hundreds of lncRNAs are differentially expressed in thyroid cancer tissues when compared with normal tissues. By copy number variation analyses, we identified that some of those dysregulated lncRNAs genome locus are accompanied with the copy number amplification or deletion. Moreover, some lncRNAs expression levels are significantly associated with thyroid cancer patients overall or recurrence‐free survival time, such as RUNDC3A‐AS1, FOXD2‐AS1, PAX8‐AS1, and CRYM‐AS1. Furthermore, we validated an lncRNA termed LINC00704 in thyroid cancer cells by performing loss of function assays. Downregulation of LINC00704 could significantly impair thyroid cancer cells proliferation, colony formation, inhibit cell‐cycle progression and cell invasion, and induce cell apoptosis. Taken together, our findings reveal that lots of lncRNAs are dysregulated and may play critical roles in thyroid cancer, and this study could provide useful resource for identification and investigation of novel lncRNA candidates for thyroid cancer.

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MALAT1 promotes the proliferation and invasion of thyroid cancer cells via regulating the expression of IQGAP1

Cited by 64 publications

References 28 publications

MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR

MALAT1 Long Non-coding RNA Expression in Thyroid Tissues: Analysis by In Situ Hybridization and Real-Time PCR

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Identification of differential expressed lncRNAs in human thyroid cancer by a genome‐wide analyses

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