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

Luan, Chunyan; Li, Yongzhu; Liu, Zhigang; Zhao, Cunxin

doi:10.2147/ott.s242300

Cited by 17 publications

(15 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Applying in vitro experiments using clinical cancer tissues and cancer cell lines, we observed that overexpression of the lncRNA MALAT1 in EOC cells encouraged drug resistance, invasion, and migration through adaptive remodeling strategies that promote tumor cell survival and proliferation, combined with the inhibition of cellular immunity and apoptosis in the TME, hence triggering EOC tumor progression. Our investigation also revealed that MALAT1 was highly expressed among carcinoma tissues from various organs, including EOCs, as previously reported [ 26 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ]. Mechanistically, the activity of MALAT1 in transcriptional regulation showed that MALAT1-knockdown inhibited the oncogenic function in RCC and consistently depleted histone methyltransferase e nhancer of z este h omology 2 (EZH2), a histone lysine N-methyltransferase enzyme (EC 2.1.1.43), resulting in the inhibition of the EMT through the recovery of E-cadherin and a downregulation of β-catenin [ 40 ].…”

Section: Discussionsupporting

confidence: 89%

LncRNA MALAT1 Facilitates Ovarian Cancer Progression through Promoting Chemoresistance and Invasiveness in the Tumor Microenvironment

Mao

Fan

Dlamini

et al. 2021

IJMS

View full text Add to dashboard Cite

Upregulation of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1, also known as nuclear-enriched abundant transcript 2 (NEAT2) or LINC00047) was found in various solid tumors, including epithelial ovarian cancer (EOC). MALAT1 is a long noncoding (lnc)RNA that regulates many functional signaling pathways, including tumorigenesis. Herein, we observed the consistent upregulation of MALAT1 in MYST4-overexpressing cell lines, while MALAT1 was frequently found to be upregulated in various types of clinical carcinoma tissues, especially EOC. To further investigate the lncRNA MALAT1 in EOC progression, the transduced overexpression of MALAT1 in EOC cell lines and cancer-associated fibroblasts (CAFs) was employed. We found that MALAT1 overexpression in EOC cell lines significantly increased drug resistance, cell migration, and invasion. Furthermore, the concomitant overexpression of MALAT1 in EOC cells and CAFs dramatically increased EOC cell invasion. Accordingly, a mechanistic investigation of MALAT1 overexpression in EOC cells showed that expressions of the cytokines interleukin (IL)-1β and p-P38/p-NFκB/Cox2/prostaglandin E2 (PGE2) signaling were significantly increased, which stimulated inflammatory responses, whereas cell apoptosis was inhibited due to increased Bcl-2 levels and reduced Caspase3 levels. After MALAT1 was overexpressed in EOC cells, and the cyclin D1, p-PI3K, and p-Akt expressions increased, suggesting the promotion of tumor cell proliferation, while increased zinc finger E-box-binding homeobox-2 (ZEB2), yes-associated protein (YAP), and vimentin expression with E-cadherin downregulation indicated the enhancement of the epithelial-to-mesenchymal transition (EMT) in terms of metastasis, thereby triggering EOC progression. Together, our findings demonstrate how MALAT1 overexpression facilitates an oncogenic function through inhibiting tumor cell apoptosis, combined with increasing tumor cell inflammation, proliferation, and invasion in the EOC tumor microenvironment. MALAT1 is thus a potential diagnostic marker and therapeutic for this malignancy.

show abstract

Section: Discussionsupporting

confidence: 89%

LncRNA MALAT1 Facilitates Ovarian Cancer Progression through Promoting Chemoresistance and Invasiveness in the Tumor Microenvironment

Mao

Fan

Dlamini

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…Another study demonstrated that STC1 can promote the invasion of breast cancer cells [ 43 ]. In colon cancer, the lncRNA-MALAT1/miR-101-3p/STC1 axis can promote the development of the tumor [ 44 ]. So, STC1 was regarded as the potential candidate for further analysis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analyses of Stromal-Immune Score-Related Competing Endogenous RNA Networks In Colon Adenocarcinoma

Tong

Peng

et al. 2022

Disease Markers

View full text Add to dashboard Cite

Although recent clinical investigations emphasize the roles of myriad diversities of RNAs in stromal and immune components in the tumor microenvironment, especially in colon adenocarcinoma, however, analyses of “competing endogenous RNAs (ceRNA)” network in association with stromal and immune scores have yet to be determined. This study was conducted to explore the regulatory mechanisms of a stromal-immune score-based ceRNA network in colon adenocarcinoma. Stromal and immune scores of colon adenocarcinoma tumor samples were calculated by using the ESTIMATE algorithm. Differential expression analysis between samples with high/low stromal and immune scores was performed, followed by functional annotation for the overlapping DEmRNAs. The ceRNA network was constructed by differential expression analysis, prediction of RNA-RNA interaction, and correlation with clinicopathological parameters of the patients, which were further verified by external datasets and experiments. Colon adenocarcinoma patients having higher immune scores exhibited prolonged overall survival. RNA dataset analyses from TCGA revealed aberrant expressions of a total of 2052 mRNAs, 108 lncRNAs, and 70 miRNAs between high and low stromal/immune groups. Functional annotation mapped the differentially overexpressed mRNAs for immune-associated GO terms. To construct the ceRNA network, a total of 48 lncRNAs, 40 miRNAs, and 199 mRNAs were sorted out. A dysregulated ceRNA network consisting of 6 lncRNAs, 11 miRNAs, and 39 mRNAs was constructed by comparing RNA expressions between cancer as well as adjacent normal tissues. The ceRNA regulatory axis “MIAT/miR-532-3p/STC1” was regarded as a potential hit by the comprehensive analysis. The RT-qPCR assay showed upregulation of MIAT and STC1 while downregulation of hsa-miR-532-3p expression in cancer. Thus, our study highlights the potential role of a stromal-immune score-based ceRNA network in the colon adenocarcinoma microenvironment. The ceRNA axis MIAT/miR-532-3p/STC1 could serve as a promising therapeutic target for colon adenocarcinoma.

show abstract

“…These studies suggest that miR-101–3p may be an important tumour-associated gene, with potential in drug development. In LC, miR-101–3p has generally been studied as a common targeting site for long-noncoding-RNA MALAT1 [ 8 ] or SNHG6 [ 16 ], implying that it may have an important therapeutic role. However, its expression level and actual therapeutic effect in LC, as well as its oncological therapeutic mechanism, have not been reported.…”

Section: Discussionmentioning

confidence: 99%

Nanomedicine promotes ferroptosis to inhibit tumour proliferation in vivo

Luo

Niu

et al. 2021

Redox Biology

View full text Add to dashboard Cite

miR-101–3p may play a therapeutic role in various tumours. However, its anti-tumour mechanism remains unclear, and a definitive strategy to treat tumour cells in vivo is lacking. The objective of this study was to investigate the inhibitory mechanism of miR-101–3p on tumour cells and to develop relevant nanomedicines for in vivo therapy. The expression levels of miR-101–3p and its target protein TBLR1 in tumour tissues and cells were detected, and their relationship with ferroptosis was clarified. Furthermore, the efficacy of nanocarriers in achieving in vivo therapeutic gene delivery was evaluated. Nanomedicine was further developed, with the anti-proliferative in vivo therapeutic effect validated using a subcutaneous xenograft cancer model. The expression level of miR-101–3p negatively correlated with clinical tumour size and TNM stage. miR-101–3p restores ferroptosis in tumour cells by directly targeting TBLR1, which in turn promotes apoptosis and inhibits proliferation. We developed nanomedicine that can deliver miR-101–3p to tumour cells in vivo to achieve ferroptosis recovery, as well as to inhibit in vivo tumour proliferation. The miR-101–3p/TBLR1 axis plays an important role in tumour ferroptosis. Nanopharmaceuticals that increase miR-101–3p levels may be effective therapies to inhibit tumour proliferation.

show abstract

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

Cited by 17 publications

References 49 publications

LncRNA MALAT1 Facilitates Ovarian Cancer Progression through Promoting Chemoresistance and Invasiveness in the Tumor Microenvironment

LncRNA MALAT1 Facilitates Ovarian Cancer Progression through Promoting Chemoresistance and Invasiveness in the Tumor Microenvironment

Comprehensive Analyses of Stromal-Immune Score-Related Competing Endogenous RNA Networks In Colon Adenocarcinoma

Nanomedicine promotes ferroptosis to inhibit tumour proliferation in vivo

Contact Info

Product

Resources

About