Silencing of lncRNA ZFAS1 inhibits malignancies by blocking Wnt/β-catenin signaling in gastric cancer cells

Xu, W.; He, Liang; Liu, Ying; Tan, Yan; Zhang, Fan; Xu, Hong

doi:10.1080/09168451.2018.1431518

Cited by 83 publications

(74 citation statements)

References 32 publications

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“…qRT-PCR results revealed that LncRNAZFAS1 was significantly up-regulated in NSCLC-related tissues and cells, compared with relative normal tissues and cells. Similar results were investigated in nasopharyngeal carcinoma, colorectal cancer (CRC) and gastric cancer (Thorenoor et al 2016;Fang et al 2017;Chen et al 2018;Xie et al 2018;Xu et al 2018). To indicate the relationship between the expression level of LncRNAZFAS1 and tumor stage and metastasis, we found that LncRNAZFAS1 was significantly overexpressed in stage III / IV and in metastatic NSCLC tissues, further indicating that elevated LncRNAZ-FAS1 was remarkably correlated with TNM stage and lymph node metastasis and may promote the progression and metastasis of NSCLC.…”

Section: Discussionsupporting

confidence: 75%

Knockdown of LncRNAZFAS1 suppresses cell proliferation and metastasis in non-small cell lung cancer

Zhou

Yang

et al. 2020

Animal Cells and Systems

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To evaluate the effects of LncRNAZFAS1 on cell proliferation and tumor metastasis in non-small cell lung cancer (NSCLC), we detected the expression level of LncRNAZFAS1 in NSCLC-related tissues and cells. qRT-PCR results revealed that LncRNAZFAS1 in tumor tissues was significantly higher than that in normal lung tissue, especially significantly up-regulated in stage III / IV and in metastatic NSCLC tissues. LncRNAZFAS1 expression was dramatically up-regulated in 4 NSCLCrelated cells (A549, SPC-A1, SK-MES-1, and NCI-H1299), with having the highest expression level in A549 cells. Furthermore, we implemented a knockdown of LncRNAZFAS1 in A549 cells, and the results of CCK8 and Transwell assays suggested that knockdown of LncRNAZFAS1 significantly inhibited NSCLC cell proliferation and metastasis. Next, we constructed a tumor xenograft model to evaluate the effect of LncRNAZFAS1 on the NSCLC cell proliferation in vivo. The results indicated that knockdown of LncRNAZFAS1 dramatically inhibited A549 cells proliferation and repressed tumor growth. Additionally, knockdown of LncRNAZFAS1 drastically weakened the expressions of MMP2, MMP9 and Bcl-2 proteins, whereas noticeably strengthened the expression of BAX protein. Our results altogether suggest that knockdown of LncRNAZFAS1 has a negative effect on the proliferation and metastasis of NSCLC cell, which implying LncRNAZFAS1 is a potential unfavorable biomarker in patients with NSCLC.

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Section: Discussionsupporting

confidence: 75%

Knockdown of LncRNAZFAS1 suppresses cell proliferation and metastasis in non-small cell lung cancer

Zhou

Yang

et al. 2020

Animal Cells and Systems

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“…For instance, ZFAS1 was found to promote resistance to Adriamycin in T-cell acute lymphoblastic leukemia [45]. ZFAS1 knockdown led to significantly impaired resistance to cis-platinum or paclitaxel in gastric cancer [46]. Increased resistance to temozolomide in glioma [47].…”

Section: Discussionmentioning

confidence: 99%

LncRNA ZFAS1 contributed to irradiation resistance in nasopharyngeal carcinoma by inhibiting hsa-miR-7-5p/ENO2

Peng

Feng

Zheng

et al. 2020

Preprint

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Background: In our previous research, we found that lncRNA ZFAS1 could promote nasopharyngeal carcinoma by inhibiting its downstream target axis. But we hadn’t shown whether ZFAS1 had association with irradiation resistance of NPC. In this study, we aimed to study the role of ZFAS1 in irradiation resistance of nasopharyngeal carcinoma. Methods: Bioinformatics analysis was first conducted to identify the potentially significant gene that participated in radio resistance of nasopharyngeal carcinoma. qRT-PCR was used to detect the expression of ZFAS1, miR-7-5p and ENO2 mRNA. The location of ZFAS1 was measured in cell fractions. The relationship between ZFAS1, miR-7-5p and ENO2 mRNA was validated by luciferase reporter assay and RNA pull down. Edu assay and flow cytometric apoptosis assay were conducted to observe how ZFAS1, miR-7-5p and ENO2 affected nasopharyngeal carcinoma proliferation and apoptosis under irradiation. Results：ZFAS1 was upregulated in nasopharyngeal carcinoma, which was associated with radio resistance. ZFAS1 strengthened the ability of irradiation resistance in nasopharyngeal carcinoma. ZFAS1 acted on miR-7-5p to promote ENO2 upregulation, thereby promoting the irradiation resistance. Conclusion: ZFAS1 sponged miR-7-5p to further affect ENO2 expression to augmenting the irradiation resistance in nasopharyngeal carcinoma.

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“…A number of reports have indicated that lncRNAs serve important functions in the regulation of biological processes, including proliferation, cell survival and cell mobility (23). LncRNAs are widely involved in tumorigenesis (24) and a number of lncRNAs have been reported to regulate BC progression (25,26). Li et al (27) reported that lncRNA ANCR regulated EZH2 degradation and attenuated the invasion and metastasis of BC.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA EZR‑AS1 promotes tumor growth and metastasis by modulating Wnt/β‑catenin pathway in breast cancer

Bai

Zhou

et al. 2018

Exp Ther Med

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Accumulating evidence has demonstrated that long noncoding RNAs (lncRNAs) serve important roles in tumor development and progression. However, whether lncRNA EZR-AS1 is associated with breast cancer (BC) progression remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction analysis demonstrated that the expression of EZR-AS1 was significantly upregulated in BC tissues and cell lines. Furthermore, Kaplan-Meier curve analysis revealed that increased EZR-AS1 expression in patients with BC contributes to poor prognosis. Cell counting kit-8 and fluorescence-activated cell sorting experiments indicated that EZR-AS1 knockdown significantly suppressed the proliferation and cell cycle progression of breast cancer cells, while reducing cellular apoptosis. Furthermore, Transwell assays suggested that EZR-AS1 knockdown reduced the migration and invasion ability of BC cells compared with control cells. In the present study, it was observed that EZR-AS1 interacts with β-catenin to prevent degradation. EZR-AS1 knockdown resulted in β-catenin downregulation and inactivation of the Wnt/β-catenin pathway. Rescue assays revealed that β-catenin overexpression reversed the effects of EZR-AS1 knockdown on BC cell proliferation, apoptosis, migration and invasion. In conclusion, the results of the present study demonstrate that EZR-AS1 serves as an oncogene in BC via activating the Wnt/β-catenin pathway. This suggests that EZR-AS1 may be a therapeutic target for BC treatment.

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Silencing of lncRNA ZFAS1 inhibits malignancies by blocking Wnt/β-catenin signaling in gastric cancer cells

Cited by 83 publications

References 32 publications

Knockdown of LncRNAZFAS1 suppresses cell proliferation and metastasis in non-small cell lung cancer

Knockdown of LncRNAZFAS1 suppresses cell proliferation and metastasis in non-small cell lung cancer

LncRNA ZFAS1 contributed to irradiation resistance in nasopharyngeal carcinoma by inhibiting hsa-miR-7-5p/ENO2

Long noncoding RNA EZR‑AS1 promotes tumor growth and metastasis by modulating Wnt/β‑catenin pathway in breast cancer

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