Long non‐coding RNA FEZF1‐AS1 promotes breast cancer stemness and tumorigenesis via targeting miR‐30a/Nanog axis

Zhang, Zhi; Sun, Liwei; Zhang, Yixuan; Lu, Guan-Ming; Li, Yongqiang; Wei, Zhongheng

doi:10.1002/jcp.26611

Cited by 61 publications

(52 citation statements)

References 31 publications

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“…Known to be highly expressed in various cancers, FEZF1-AS1 is involved in cell proliferation, migration, invasion and the Warburg Effect [103]. FEZF1-AS1 increases the expression of stem cell markers NANOG, OCT4 and SOX2 in MDA-MD-231 TNBC cells by acting as ceRNA sponging miR-39a [80].…”

Section: Fezf1-as1mentioning

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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Section: Fezf1-as1mentioning

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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“…13,14,16 For instance, FEZF1-AS1 is upregulated in breast cancer can target miR-30a/Nanog axis to increase cancer cell stemness. 14 In another study, Zhao et al reported that FEZF1-AS1 was overexpressed in ovarian cancer can promote cancer cell proliferation and inhibited cancer cell apoptosis through the activation of JAK-STAT3 pathway. 16 In this study, we observed the upregulation of FEZF1-AS1 in GBM.…”

Section: Discussionmentioning

confidence: 99%

“…12 Long non-coding RNA (lncRNA) FEZF1-AS1 has been characterized as an oncogenic lncRNA in several types of cancers, such as colorectal carcinoma and breast cancer. 13,14 However, its involvement in GBM is unknown. We analyze TCGA dataset and observed the upregulation of FEZF1-AS1 in GBM.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA FEZF1-AS1 Sponges miR-34a to Upregulate Notch-1 in Glioblastoma</p>

Luo¹,

Zhang²,

He³

et al. 2020

CMAR

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Introduction: LncRNA FEZF1-AS1 has been reported to be an oncogene in many types of cancer, while its role in glioblastoma (GBM) is unknown. This study aimed to investigate the potential involvement of FEZF1-AS1 in GBM. Methods: FEZF1-AS1 expression in paired GBM and non-tumor tissues from GBM patients was determined by RT-qPCR. A 2-year follow-up was performed to analyze the prognostic value of FEZF1-AS1 for GBM. Cell transfections were performed to analyze the interactions between FEZF1-AS1, miR-34a and Notch-1. Transwell assay was performed to analyze the role of FEZF1-AS1, miR-34a and Notch-1 in regulating GBM cell invasion and migration. Results: In this study, analysis of TCGA dataset revealed the upregulation of FEZF1-AS1 in GBM, and the overexpression of FEZF1-AS1 in GBM was further confirmed using GBM tissues from GBM patients included in this study. High levels of FEZF1-AS1 were correlated with poor survival. FEZF1-AS1 was predicted to form base pairing with miR-34a. However, overexpression of FEZF1-AS1 and miR-34a failed to affect the expression of each other. However, upregulation of Notch-1, a target of miR-34a, was observed after FEZF1-AS1 in GBM cells. Moreover, increased invasion and migration rates of GBM cells were observed after FEZF1-AS1 and Notch-1 overexpression. MiR-34a played an opposite role and reduced the effects of FEZF1-AS1 and Notch-1 overexpression. Conclusion: FEZF1-AS1 may sponge miR-34a to upregulate Notch-1 in GBM, thereby promoting cancer cell invasion and migration.

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“…Silencing of LncRNA n339260 reduces the stemness of HCC cells . Zhang reported that lncRNA FEZF1‐AS1 regulates breast cancer stem cells by sponging miR‐30a, which targets Nanog …”

Section: Discussionmentioning

confidence: 99%

“…32 Zhang reported that lncRNA FEZF1-AS1 regulates breast cancer stem cells by sponging miR-30a, which targets Nanog. 33 Several studies have indicated that lncRNA SPRY4-IT1 is associated with the progress of breast cancer. LncRNA SPRY4-IT1 is highly expressed in breast cancer cells, and N-terminal polypeptide derived from viral macrophage inflammatory protein Ⅱ (NT21MP) inhibits the biological functions of breast cancer cells through lncRNA SPRY4-IT1.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2

Song

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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SPRY4‐intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4‐IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4‐IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT‐PCR to detect the expression of SPRY4‐IT1 in MCF‐7 cells and MCF‐7 cancer stem cells (MCF‐7 CSCs). The effects of SPRY4‐IT1 on the proliferation and renewal ability of breast cancer cells were investigated by in vitro and in vivo assays (ie in situ hybridization, colony formation assay, sphere formation assay, flow cytometry assay, western blotting, xenograft model and immunohistochemistry). The mechanism of SPPRY4‐IT1 as a ceRNA was studied by a dual‐luciferase reporter assay and bioinformatic analysis. In our study, SPRY4‐IT1 was up‐regulated in MCF‐7 CSCs compared with MCF‐7 cells, and high SPRY4‐IT1 expression was related to reduced breast cancer patient survival. Furthermore, SPRY4‐IT1 overexpression promoted breast cancer cell proliferation and stemness in vitro and in vivo. In addition, SPRY4‐IT1 knockdown suppressed BCSC renewal ability and stemness maintenance in vivo and in vitro. The dual‐luciferase reporter assays indicated that SPRY4‐IT1 as a sponge for miR‐6882‐3p repressed transcription factor 7‐like 2 (TCF7L2) expression. Taken together, these findings demonstrated that SPRY4‐IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR‐6882‐3p.

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Long non‐coding RNA FEZF1‐AS1 promotes breast cancer stemness and tumorigenesis via targeting miR‐30a/Nanog axis

Cited by 61 publications

References 31 publications

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

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

<p>LncRNA FEZF1-AS1 Sponges miR-34a to Upregulate Notch-1 in Glioblastoma</p>

LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2

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