CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Han, Chunyong; Li, Xuebiao; Fan, Qian; Liu, Guangshu; Yin, Jian

doi:10.18632/aging.102080

Cited by 56 publications

(40 citation statements)

References 54 publications

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“…It is now well established that lncRNAs are important regulators of human diseases. Previous studies have shown that lncRNA CCAT1 is upregulated in a series of cancers, including colorectal cancer (Nissan et al, 2012), non-small cell lung cancer (Luo et al, 2014), breast cancer (Han et al, 2019), hepatocellular carcinoma (Guo et al, 2019), gastric cancer (Li Y. et al, 2019), gallbladder cancer (Ma et al, 2015), acute myeloid leukemia (Chen et al, 2016), endometrial carcinoma (Yu et al, 2019), nasopharyngeal carcinoma (Dong et al, 2018), and cervical cancer (Shen et al, 2019). In this study, we found that the expression of CCAT1 was significantly increased in LAD tissues than that of adjacent non-tumor tissues.…”

Section: Discussionsupporting

confidence: 52%

“…LncRNA colon cancer-associated transcript-1(CCAT1) was significantly upregulated in colon cancer tissue and cells (Nissan et al, 2012). Recently, CCAT1 has been studied in various cancers (Guo and Hua, 2017;Shi et al, 2017;Han et al, 2019;Hu et al, 2019;. CCAT1 plays a role in promoting the proliferation and invasion of cervical cancer by regulating the miR-181a-5p/MMP14 axis (Shen et al, 2019) and promotes endometrial carcinoma progression by miR-181a-5p (Yu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1

et al. 2020

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Previous evidence suggests that long non-coding colon cancer-associated transcript-1(CCAT1) plays a pivotal role in the progression of a variety of tumors. However, little is known about its role in lung adenocarcinoma (LAD). In this study, we found LAD tissue samples had a higher expression of CCAT1 but a lower expression of miR-219-1 compared to their adjacent non-tumor tissues. CCAT1 negatively regulated the expression of miR-219-1. miR-219-1 suppressed the proliferation of A549 and H1299 cells. Knockdown of CCAT1 inhibited the proliferation, migration, and invasion of A549 and H1299 cells, which were reversed by the miR-219-1 inhibitor. CCAT1 knockdown increased the expression of E-cadherin but decreased the expressions of N-cadherin and vimentin, which were restored by the miR-219-1 inhibitor. In vivo, knockdown of CCAT1 suppressed the tumor growth of LAD xenografts, which were rescued by the inhibition of miR-219-1. In summary, our findings suggested that CCAT1 promotes the progression of LAD via sponging miR-219-1, providing a potential therapeutic target for LAD.

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Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1

et al. 2020

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“…Colon cancer-associated transcript-1 (CCAT1) was first studied in colon cancer and subsequently in other cancers, including breast cancer [75,101]. In spheroid culture, breast cancer cells had a higher expression of CCAT1 [74].…”

Section: Ccat1mentioning

confidence: 99%

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

Brown

Wasson

Marcato

2020

Cells

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Treatment decisions for breast cancer are based on staging and hormone receptor expression and include chemotherapies and endocrine therapy. While effective in many cases, some breast cancers are resistant to therapy, metastasize and recur, leading to eventual death. Higher percentages of tumor-initiating cancer stem cells (CSCs) may contribute to the increased aggressiveness, chemoresistance, and worse outcomes among breast cancer. This may be particularly true in triple-negative breast cancers (TNBCs) which have higher percentages of CSCs and are associated with worse outcomes. In recent years, increasing numbers of long non-coding RNAs (lncRNAs) have been identified as playing an important role in breast cancer progression and some of these have been specifically associated within the CSC populations of breast cancers. LncRNAs are non-protein-coding transcripts greater than 200 nucleotides which can have critical functions in gene expression regulation. The preclinical evidence regarding lncRNA antagonists for the treatment of cancer is promising and therefore, presents a potential novel approach for treating breast cancer and targeting therapy-resistant CSCs within these tumors. Herein, we summarize the lncRNAs that have been identified as functionally relevant in breast CSCs. Furthermore, our review of the literature and analysis of patient datasets has revealed that many of these breast CSC-associated lncRNAs are also enriched in TNBC. Together, this suggests that these lncRNAs may be playing a particularly important role in TNBC. Thus, certain breast cancer-promoting/CSC-associated lncRNAs could be targeted in the treatment of TNBCs and the CSCs within these tumors should be susceptible to anti-lncRNA therapy.

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“…The ceRNA pattern was widely observed in TNBC progression. Silenced CCAT1 inhibited TNBC cell proliferation, migration, and invasion through endogenously sponging miR-218 to elevate ZFX expression 2 . LINC01133 promotes phenotypic and growth characteristics of cancer stem cell-like cells via mediating the miR-199a/FOXP2 axis in TNBC cells 3 .…”

Section: Introductionmentioning

confidence: 99%

M2 macrophage-induced lncRNA PCAT6 facilitates tumorigenesis and angiogenesis of triple-negative breast cancer through modulation of VEGFR2

et al. 2020

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As a common female malignancy, triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancers (BC). This study further studied the role of long noncoding RNA (lncRNA) prostate cancer-associated transcript 6 (PCAT6) in TNBC. Functional assays, including EdU, wound healing, transwell, and immunofluorescence staining, revealed the effect of PCAT6 on cell proliferation, migration, and EMT process. The tube-formation assay disclosed the function of PCAT6 on angiogenesis. In vivo assays were also established to explore the impact of PCAT6 on tumor growth and microangiogenesis. The results revealed that PCAT6 boosted TNBC cell proliferation, migration, and angiogenesis both in vitro and in vivo. Then, this study unveiled that M2 macrophage secreted VEGF to stimulate the upregulation of PCAT6, thus promoting angiogenesis in TNBC. Next, through bioinformatics analysis and mechanism assays, we identified that PCAT6 positively regulated VEGFR2 expression via ceRNA pattern and then participated in VEGFR/AKT/mTOR signaling pathway to accelerate angiogenesis. Moreover, PCAT6 bound USP14, a deubiquitinase, to induce the deubiquitination of VEGFR2. On the whole, M2 macrophage-induced upregulation of PCAT6 facilitates TNBC tumorigenesis through modulation of VEGFR2 expression via ceRNA and deubiquitination patterns.

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CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Cited by 56 publications

References 54 publications

Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1

Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

M2 macrophage-induced lncRNA PCAT6 facilitates tumorigenesis and angiogenesis of triple-negative breast cancer through modulation of VEGFR2

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