Novel insight into MALAT-1 in cancer: Therapeutic targets and clinical applications

Ren, Danyang; Li, Huiying; Li, Renqiu; Sun, Jianming; Guo, Peng; Han, Hui-yun; Yang, Ying; Li, Jun

doi:10.3892/ol.2016.4138

Cited by 29 publications

(23 citation statements)

References 83 publications

(116 reference statements)

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“…Since its discovery, several studies have reported the link of MALAT-1 to other cancers, including gallbladder-, cervical-, non-small cell lung- (NSCLC), colorectal-, and breast cancer. In most cases, MALAT-1 is upregulated in cancer and is associated with metastasis, cell proliferation, apoptosis, and migration, as well as with clinically unfavorable prognostic parameters [ 16 , 49 , 103 , 104 , 105 , 106 ].…”

Section: Lncrna Candidates In Breast Cancermentioning

confidence: 99%

Current Status of Long Non-Coding RNAs in Human Breast Cancer

Cerk

Schwarzenbacher

Adiprasito

et al. 2016

IJMS

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Breast cancer represents a major health burden in Europe and North America, as recently published data report breast cancer as the second leading cause of cancer related death in women worldwide. Breast cancer is regarded as a highly heterogeneous disease in terms of clinical course and biological behavior and can be divided into several molecular subtypes, with different prognosis and treatment responses. The discovery of numerous non-coding RNAs has dramatically changed our understanding of cell biology, especially the pathophysiology of cancer. Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts >200 nucleotides in length. Several studies have demonstrated their role as key regulators of gene expression, cell biology and carcinogenesis. Deregulated expression levels of lncRNAs have been observed in various types of cancers including breast cancer. lncRNAs are involved in cancer initiation, progression, and metastases. In this review, we summarize the recent literature to highlight the current status of this class of long non-coding lncRNAs in breast cancer.

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Section: Lncrna Candidates In Breast Cancermentioning

confidence: 99%

Current Status of Long Non-Coding RNAs in Human Breast Cancer

Cerk

Schwarzenbacher

Adiprasito

et al. 2016

IJMS

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“…Single cell RNASeq analyses showed high levels of expression of various metastasis-related markers (particularly the MIF/CD44/CD74/CXCR4 signaling axis), as well as LINE-1 retrotransposons. In addition, the MTFs uniformly expressed very high levels of MALAT1, a long non-coding RNA transcript known to be involved in control of metastasis [ 25 , 26 ], as well as additional long non-coding transcripts implicated in cancer progression. When the cultured PDAC MTFs were orthotopically transplanted into the pancreas in mice, they formed well-differentiated islands there.…”

Section: Introductionmentioning

confidence: 99%

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

et al. 2017

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Here we describe isolation and characterization of macrophage-tumor cell fusions (MTFs) from the blood of pancreatic ductal adenocarcinoma (PDAC) patients. The MTFs were generally aneuploidy, and immunophenotypic characterizations showed that the MTFs express markers characteristic of PDAC and stem cells, as well as M2-polarized macrophages. Single cell RNASeq analyses showed that the MTFs express many transcripts implicated in cancer progression, LINE1 retrotransposons, and very high levels of several long non-coding transcripts involved in metastasis (such as MALAT1). When cultured MTFs were transplanted orthotopically into mouse pancreas, they grew as obvious well-differentiated islands of cells, but they also disseminated widely throughout multiple tissues in “stealth” fashion. They were found distributed throughout multiple organs at 4, 8, or 12 weeks after transplantation (including liver, spleen, lung), occurring as single cells or small groups of cells, without formation of obvious tumors or any apparent progression over the 4 to 12 week period. We suggest that MTFs form continually during PDAC development, and that they disseminate early in cancer progression, forming “niches” at distant sites for subsequent colonization by metastasis-initiating cells.

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“…In another study, the MALAT1 sequence was infused into mice pulmonary carcinoma and the tumor growth and metastasis was inhibited (Gutschner et al, 2013b). Compared to primary tumors, the level of MALAT1 was further elevated in metastatic tumors, suggesting a correlation between the levels of MALAT1 and malignant tumors (Ren et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells

Zhang¹,

Huerxidan²,

Zhao³

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Cervical cancer is a common female malignancy of global dimensions. MicroRNAs (miRNAs) play crucial roles in the development, differentiation, proliferation, and apoptosis of tumors. The non-coding RNA MALAT1 participates in various physiological processes that are important for proper functioning of the body. Here, we analyzed the expression of miRNA-143 and MALAT1 in HeLa cells to evaluate their roles in the occurrence and metastasis of cervical cancer. HeLa cells were divided into five groups depending on the treatment conditions, namely, transfected with miRNA-143, MALAT1, miRNA-143 inhibitor and the MALAT1 inhibitor, and the untreated control. Reverse transcription-polymerase chain reaction was used to analyze the expression of miRNA-143 and MALAT1, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to assess proliferation, the trans-well assay to study cell invasion and migration, and western blot to analyze the levels of E-cadherin and vimentin. The proliferation of HeLa cells increased upon treatment with the miRNA-143 inhibitor and decreased when treated with the MALAT1 inhibitor, compared to the proliferation of the groups that were transfected with miRNA-143 and MALAT1, respectively (P < 0.05). Thus, miRNA-143 decreased cell invasion and migration potency, downregulated vimentin and upregulated E-cadherin expression, while MALAT1 had the opposite effects. In conclusion, the low expression of miRNA-143 and high expression of MALAT1 in cervical cancer cells could possibly potentiate cell invasion/migration and alter the levels of vimentin and E-cadherin.

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Novel insight into MALAT-1 in cancer: Therapeutic targets and clinical applications

Cited by 29 publications

References 83 publications

Current Status of Long Non-Coding RNAs in Human Breast Cancer

Current Status of Long Non-Coding RNAs in Human Breast Cancer

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells

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