LncRNA DSCAM‐AS1 acts as a sponge of miR‐137 to enhance Tamoxifen resistance in breast cancer

Ma, Yun; Bu, Deyong; Jiang, Long; Chai, Wenying; Dong, Jian

doi:10.1002/jcp.27105

Cited by 54 publications

(42 citation statements)

References 34 publications

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“…Recently studies showed that miR-137 might participate in the progression of CRC by directly targeting at EZH2 [32], TCF4 [31] and YBX1 [33]. Study showed that DSCAM-AS1 may act as a competing endogenous RNA of miR-137 and regulates EPS8 to promote cell reproduction and suppresses cell apoptosis in TR breast cancer [34]. RT-qPCR results in our study displayed that the expression of miR-137 in CRC tissues was relatively lower than that in normal tissues, and was negatively correlated with the expression of DSCAM-AS1.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Xu¹,

Wu²,

Zhao³

et al. 2020

J. Cancer

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Growing evidences demonstrate that long noncoding RNAs (lncRNAs) participate in various cancers including colorectal cancer (CRC). In the current study, we found that the expression of DSCAM-AS1 in CRC tissues and cell lines was significantly upregulated, and was positively correlated with metastasis status and advanced stage of CRC. In addition, Kaplan-Meier assays also indicated that the expression of DSCAM-AS1 was correlated with poor prognosis in patients with CRC. Silence of DSCAM-AS1 inhibited proliferation and migration of CRC cells. Subcellular fractionation and FISH analyses suggested that DSCAM-AS1 was majorly distributed in cytoplasm of HT29 and LOVO cells. Thus, DSCAM-AS1 might act as a competing endogenous RNA (ceRNA). Subsequently, RT-qPCR results displayed that the expression of miR-137 in CRC tissues was relatively lower than that in the neighboring normal tissues. The interaction between miR-137 and DSCAM-AS1 was demonstrated by luciferase reporter assay. Functionally, miR-137 reversed the pro-proliferation and-metastasis effect of DSCAM-AS1 on CRC cells. Collectively, DSCAM-AS1 promotes CRC progression via sponging miR-137. MiR-137 can suppress the expression of Notch-1, a novel signaling regulating cell proliferation and EMT, by working on the 3'UTR of Notch-1. At last, Notch-1 overexpression or miR-137 inhibition could restore the DSCAM-AS1 silencing-mediated repressive function on cell proliferation and migration. The above data suggested that, DSCAM-AS1 may contribute to CRC cell proliferation and migration by targeting miR-137/Notch-1 axis.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Xu¹,

Wu²,

Zhao³

et al. 2020

J. Cancer

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“…The Down syndrome cell adhesion molecule antisense RNA 1 (DSCAM-AS1) is an intronic antisense lncRNA that is transcribed from the opposite strand of the Down syndrome cell adhesion molecule (DSCAM) gene, and is wholly derived from the intronic region of DSCAM. DSCAM-AS1 promotes tamoxifen resistance [110,111] and is upregulated in breast cancer tissues compared with normal tissues [110,112]. Moreover, DSCAM-AS1 expression is higher in luminal and HER2-positive breast cancers, and particularly in the luminal B subtype [110,112].…”

Section: Lncrnas Belonging To Multiple Categoriesmentioning

confidence: 99%

Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

Takeiwa

Ikeda

Mitobe

et al. 2020

Cancers

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Long noncoding RNAs (lncRNAs) are defined as RNAs longer than 200 nucleotides that do not encode proteins. Recent studies have demonstrated that numerous lncRNAs are expressed in humans and play key roles in the development of various types of cancers. Intriguingly, some lncRNAs have been demonstrated to be involved in endocrine therapy resistance for breast cancer through their own mechanisms, suggesting that lncRNAs could be promising new biomarkers and therapeutic targets of breast cancer. Here, we summarize the functions and mechanisms of lncRNAs related to the endocrine therapy resistance of breast cancer.

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“…68 TINCR sponges miR-125b and promotes TZB resistance in HER-2+ BC cells. 100 Other lncRNAs such as FTH1P3, 67 LINC00511, 69 ATB, 103 CYTOR, 81 DSCAM-AS1, 83,84 ROR, 86 ADAMTS9-AS2, 91 LINC00894-002, 92 NONHSAT101069, 29 and PRLB 77 sponge specific miRNAs to regulate drug resistance in BC.…”

Section: Cernasmentioning

confidence: 99%

<p>Long Non-Coding RNAs in Drug Resistance of Breast Cancer</p>

Du¹,

Shi²,

Xu³

et al. 2020

OTT

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Breast cancer (BC) is the most common cancer and the leading cause of death in women. Advances in early diagnosis and therapeutic strategies have decreased the mortality of BC and improved the prognosis of patients to some extent. However, the development of drug resistance has limited the success rate of systemic therapies. Long non-coding RNAs (lncRNAs) are involved in drug resistance in BC via various mechanisms, which contribute to a complex regulatory network. In this review, we summarize the latest findings on the mechanisms underlying drug resistance modulated by lncRNAs in BC. In addition, we discuss the potential clinical applications of lncRNAs as targeted molecular therapy against drug resistance in BC.

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LncRNA DSCAM‐AS1 acts as a sponge of miR‐137 to enhance Tamoxifen resistance in breast cancer

Abstract: LncRNA DSCAM-AS1 acts as a competing endogenous RNA of miR-137 and regulates EPS8 to promote cell reproduction and suppresses cell apoptosis in TR breast cancer.

Cited by 54 publications

References 34 publications

Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

<p>Long Non-Coding RNAs in Drug Resistance of Breast Cancer</p>

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