Regulatory RNAs, microRNA, long-non coding RNA and circular RNA roles in colorectal cancer stem cells

Chao, Hsiao-Mei; Wang, Teh-Wei; Chern, Edward; Hsu, Shan‐hui

doi:10.4251/wjgo.v14.i4.748

Cited by 20 publications

(13 citation statements)

References 116 publications

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“…LncRNAs are involved in multiple physiological and pathological processes, the underlying mechanisms remain largely unknown [28][29][30]. In this study, data showed that ELFN1-AS1 was signi cantly upregulated in CRC tissues and promoted immune escape of CRC cells from NK cells.…”

Section: Discussionmentioning

confidence: 83%

ELFN1-AS1 Promotes GDF15-Mediated Immune Escape of Colorectal Cancer from NK cells by Facilitating GCN5 and SND1 Association

Han

Chen

et al. 2023

Preprint

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The ability of colorectal cancer (CRC) cells to escape from natural killer (NK) cell immune surveillance leads to anti-tumor treatment failure. The long non-coding RNA (lncRNA) ELFN1-AS1 is aberrantly expressed in multiple tumors suggesting a role as an oncogene in cancer development. However, whether ELFN1-AS1 regulates immune surveillance in CRC is unclear. Here, we determined that ELFN1-AS1 enhanced the ability of CRC cells to escape from NK cell surveillance in vitro and in vivo. In addition, we confirmed that ELFN1-AS1 in CRC cells attenuated the activity of NK cell by down-regulating NKG2D and GZMB via the GDF15/JNK pathway. Furthermore, mechanistic investigations demonstrated that ELFN1-AS1 enhanced the interaction between the GCN5 and SND1 protein and this influenced H3k9ac enrichment at the GDF15 promotor to stimulate GDF15 production in CRC cells. Taken together, our findings indicate that ELFN1-AS1 in CRC cells suppresses NK cell cytotoxicity and ELFN1-AS1 is a potential therapeutic target for CRC.

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Section: Discussionmentioning

confidence: 83%

ELFN1-AS1 Promotes GDF15-Mediated Immune Escape of Colorectal Cancer from NK cells by Facilitating GCN5 and SND1 Association

Han

Chen

et al. 2023

Preprint

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“…LncRNAs control cancer development and progression by attenuating gene expression through various mechanisms [24]. The actions of lncRNAs are primarily decided on the basis of their location.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA TMEM147-AS1 serves as a microRNA-326 sponge to aggravate the malignancy of gastric cancer by upregulating SMAD5

QIN¹,

JIANG²,

ZHU³

et al. 2021

Oncology Research

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The abnormal expression of long noncoding RNAs (lncRNAs) is frequently observed in gastric cancer (GC) and considered an important driving force in GC progression. However, little is known regarding the involvement of TMEM147-AS1 in GC. Therefore, we examined TMEM147-AS1 expression in GC and determined its prognostic value. In addition, TMEM147-AS1 expression was depleted to identify the functional changes in response to TMEM147-AS1 deficiency. Using the cancer genome atlas dataset and our own cohort, we identified a strong expression of TMEM147-AS1 in GC. Increased TMEM147-AS1 levels in GC showed a significant association with poor prognosis. TMEM147-AS1 interference resulted in the inhibition of GC cell proliferation, colony-forming, migration, and invasion in vitro. Additionally, depletion of TMEM147-AS1 restricted the growth of GC cells in vivo.Mechanistically, TMEM147-AS1 functioned as a microRNA-326 (miR-326) sponge. Furthermore, SMAD family member 5 (SMAD5) was experimentally validated as the functional effector of miR-326. TMEM147-AS1 was demonstrated to sequester miR-326 away from SMAD5; consequently, knocking down TMEM147-AS1 downregulated SMAD5 levels in GC cells. The functional suppression of miR-326 or reintroduction of SMAD5 effectively reversed the attenuated behavior of GC cells caused by TMEM147-AS1 downregulation. In summary, TMEM147-AS1 exhibits tumorigenic activities in GC, which is likely the result of an altered miR-326/SMAD5 axis. Therefore, targeting TMEM147-AS1/miR-326/SMAD5 may represent a target for the treatment of GC.

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“…Furthermore, SMAD2, SMAD4, and TGF-βRII genes are markedly associated with miRNA-155 and miR-22, both of which strongly correlate with tumor properties, suggesting clinical utility in immunotherapy[ 24 ]. miR-4666-3p and miR-329 act as tumor suppressor genes, affecting TGF-βR1 and thus preventing the activation of the TGF-β1/Smad pathway[ 80 ]. Finally, miR-147 overexpression has been shown to inhibit EMT and the TGF-β/SMAD pathway in colon cancer cells[ 81 ].…”

Section: Mirnas As Regulators In Crcmentioning

confidence: 99%

Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer

Mašlanková¹,

Večurkovská²,

Rabajdová³

et al. 2022

WJG

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According to data from 2020, Slovakia has long been among the top five countries with the highest incidence rate of colorectal cancer (CRC) worldwide, and the rate is continuing to rise every year. In approximately 80% of CRC cases, allelic loss (loss of heterozygosity, LOH) occurs in the long arm of chromosome 18q. The most important genes that can be silenced by 18q LOH or mutations are small mothers against decapentaplegic homolog (SMAD) 2 and SMAD4, which are intracellular mediators of transforming growth factor (TGF)-β superfamily signals. TGF-β plays an important role in the pro-oncogenic processes, including such properties as invasion, epithelial-mesenchymal transition (commonly known as EMT), promotion of angiogenesis, and immunomodulatory effects. Several recent studies have reported that activation of TGF-β signaling is related to drug resistance in CRC. Because the mechanisms of drug resistance are different between patients in different stages of CRC, personalized treatment is more effective. Therefore, knowledge of the activation and inhibition of factors that affect the TGF-β signaling pathway is very important.

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Regulatory RNAs, microRNA, long-non coding RNA and circular RNA roles in colorectal cancer stem cells

Cited by 20 publications

References 116 publications

ELFN1-AS1 Promotes GDF15-Mediated Immune Escape of Colorectal Cancer from NK cells by Facilitating GCN5 and SND1 Association

ELFN1-AS1 Promotes GDF15-Mediated Immune Escape of Colorectal Cancer from NK cells by Facilitating GCN5 and SND1 Association

Long noncoding RNA TMEM147-AS1 serves as a microRNA-326 sponge to aggravate the malignancy of gastric cancer by upregulating SMAD5

Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer

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