MALAT1 promotes the colorectal cancer malignancy by increasing DCP1A expression and miR203 downregulation

Wu, Chen; Zhu, Xiaojie; Tao, Kaixiong; Liu, Weizhen; Ruan, Tuo; Wan, Wenze; Zhang, Chun; Zhang, Weikang

doi:10.1002/mc.22868

Cited by 47 publications

(34 citation statements)

References 39 publications

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“…Among others, MALAT1 increases tumor formation in many cancers, including gastric, gallbladder, and lung cancer in vivo [77][78][79][80]. Importantly, MALAT1 has been shown in several studies to promote colorectal cancer cell development via proliferation, migration, and invasion [81,82], and is considered a potential therapeutic target for colon cancer. MALAT-1 was significantly inhibited by all delivery methods and free drugs ( Figure 11B) compared to positive control cells.…”

Section: Inhibition Of Malat-1 Expression In Hct116 Cancer Cellsmentioning

confidence: 99%

Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles

AbouAitah

Hassan

Świderska-Środa

et al. 2020

Cancers

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Antimitotics are important anticancer agents and include the natural alkaloid prodrug colchicine (COL). However, a major challenge of using COL as an anticancer drug is its cytotoxicity. We developed a novel drug delivery system (DDS) for COL using mesoporous silica nanoparticles (MSNs). The MSNs were functionalized with phosphonate groups, loaded with COL, and coated with folic acid chitosan-glycine complex. The resulting nanoformulation, called MSNsPCOL/CG-FA, was tested for action against cancer and normal cell lines. The anticancer effect was highly enhanced for MSNsPCOL/CG-FA compared to COL. In the case of HCT116 cells, 100% inhibition was achieved. The efficiency of MSNsPCOL/CG-FA ranked in this order: HCT116 (colon cancer) > HepG2 (liver cancer) > PC3 (prostate cancer). MSNsPCOL/CG-FA exhibited low cytotoxicity (4%) compared to COL (~60%) in BJ1 normal cells. The mechanism of action was studied in detail for HCT116 cells and found to be primarily intrinsic apoptosis caused by an enhanced antimitotic effect. Furthermore, a contribution of genetic regulation (metastasis-associated lung adenocarcinoma transcript 1 (MALAT 1), and microRNA (mir-205)) and immunotherapy effects (angiopoietin-2 (Ang-2 protein) and programmed cell death protein 1 (PD-1) was found. Therefore, this study shows enhanced anticancer effects and reduced cytotoxicity of COL with targeted delivery compared to free COL and is a novel method of developing cancer immunotherapy using a low-cost small-molecule natural prodrug.

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Section: Inhibition Of Malat-1 Expression In Hct116 Cancer Cellsmentioning

confidence: 99%

Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles

AbouAitah

Hassan

Świderska-Środa

et al. 2020

Cancers

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“…By enhancing Serine/arginine-rich splicing factor kinase (SRPK)1-induced SRSF1 phosphorylation, MALAT-1 promoted CRC cell proliferation, invasion, and migration via upregulation of Protein kinase (PRK)A kinase anchor protein (AKAR)9; 79 and by acting as decoy for miR-203, MALAT-1 induced the expression of mRNAdecapping enzyme (DCP)1A, resulting in increased CRC cell proliferation, invasion, and chemoresistance. 80 Activation of the MALAT-1/miR-145/Sex determining region Y-box (Sox)9 signaling axis promotes proliferation, invasion, and migration and inhibits cell cycle progression and apoptosis in CRC. 81 CRC progression is also influenced by MALAT-1/miR-129-5p/high-mobility group box (HMGB)1 signaling.…”

Section: Lung Carcinomamentioning

confidence: 99%

Regulatory Networks of LncRNA MALAT-1 in Cancer

Fu¹,

Wang²,

Li³

et al. 2020

CMAR

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Long noncoding (lnc)RNAs are a group of RNAs with a length greater than 200 nt that do not encode a protein but play an essential role in regulating the expression of target genes in normal biological contexts as well as pathologic processes including tumorigenesis. The lncRNA metastasis-associated lung adenocarcinoma transcript (MALAT)-1 has been widely studied in cancer. In this review, we describe the known functions of MALAT-1; its mechanisms of action; and associated signaling pathways and their clinical significance in different cancers. In most malignancies, including lung, colorectal, thyroid, and other cancers, MALAT-1 functions as an oncogene and is upregulated in tumors and tumor cell lines. MALAT-1 has a distinct mechanism of action in each cancer type and is thus at the center of large gene regulatory networks. Dysregulation of MALAT-1 affects cellular processes such as alternative splicing, epithelial-mesenchymal transition, apoptosis, and autophagy, which ultimately results in the abnormal cell proliferation, invasion, and migration that characterize cancers. In other malignancies, such as glioma and endometrial carcinoma, MALAT-1 functions as a tumor suppressor and thus forms additional regulatory networks. The current evidence indicates that MALAT-1 and its associated signaling pathways can serve as diagnostic or prognostic biomarker or therapeutic target in the treatment of many cancers.

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“…17 Wu et al have shown that MALAT1-miR203-DCP1A axis is associated with the malignancy of CC. 39 Sun et al have demonstrated that MALAT1 enhances the proliferation and inhibits the apoptosis of OC cells via sponging miR-503-5p. 40 Herein, miR-101-3p was predicted to be a target gene of MALAT1 by StarBase, and this target relationship was validated by dual-luciferase reporter assay and RNA pull-down assay in CC cells.…”

Section: Dovepressmentioning

confidence: 99%

Long Noncoding RNA MALAT1 Promotes the Development of Colon Cancer by Regulating miR-101-3p/STC1 Axis

Luan¹,

Li²,

Liu³

et al. 2020

OTT

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Purpose: Colon cancer (CC) is a leading cause of cancer-related deaths worldwide. This study aimed to clarify the effect of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on CC progression and the potential mechanism. Methods: CC cell lines HCT116 and HT29 were selected for functional analysis. The expression of MALAT1, microRNA (miR)-101-3p, and stanniocalcin 1 (STC1) in CC tissues and cells were measured by quantitative reverse transcription PCR (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were measured by Cell Counting Kit-8 (CCK-8), flow cytometry, wound scratch and transwell assay, respectively. The target relationships (MALAT1 and miR-101-3p, miR-101-3p and STC1) were validated by dual-luciferase reporter and RNA pull-down assay. Results: The expression of MALAT1 was elevated in CC tissues compared with adjacent normal tissues and was associated with lymph node metastasis, depth of invasion and tumor-nodemetastasis (TNM) stage. Up-regulation of MALAT1 promoted the proliferation, migration, and invasion and inhibited the apoptosis of CC cells; while MALAT1 knockdown exhibited opposite results. MiR-101-3p was a target of MALAT1, which was negatively regulated by MALAT1. Silencing of miR-101-3p reverses the anti-tumor effect of MALAT1 knockdown on CC cells. STC1 was a target of miR-101-3p, which was negatively regulated by miR-101-3p. Silencing of STC1 reverses the tumor promoting effects of MALAT1 up-regulation and miR-101-3p downregulation on CC cells. Conclusion: MALAT1 may function as an oncogene in CC progression by affecting the miR-101-3p/STC1 axis, providing a hopeful therapeutic option for CC.

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MALAT1 promotes the colorectal cancer malignancy by increasing DCP1A expression and miR203 downregulation

Cited by 47 publications

References 39 publications

Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles

Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles

<p>Regulatory Networks of LncRNA MALAT-1 in Cancer</p>

<p>Long Noncoding RNA MALAT1 Promotes the Development of Colon Cancer by Regulating <em>miR-101-3p</em>/STC1 Axis</p>

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