Long non-coding RNA HOST2 enhances proliferation and metastasis in gastric cancer

Liu, D; Zhang, M Y; Chu, Zhonghua; Zhang, M

doi:10.4149/neo_2018_180414n238

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…Liu D reported HOST2 was highly expressed in glioma tissues and its down-regulation could inhibit the growth and invasion of glioma cells [28]. Similar results were reported in hepatocellular carcinoma [24,25], cervical cancer [26], and gastric cancer [27]. In breast cancer, function of HOST2 in MCF-7 cell (Lumina A type breast cancer cell) was reported [33].…”

Section: Discussionmentioning

confidence: 54%

“…In 2015, HOST2 was firstly reported in human ovarian cancer which is highly expressed, and function as an oncogene in epithelial ovarian cancer cells by binding to miRNA let-7b [23]. In hepatocellular carcinoma [24,25], cervical cancer [26], gastric cancer [27] and glioma [28], HOST2 was also up-regulated and played a oncogene role in tumourigenesis and development. However, there is still lack of exact mechanisms about how HOST2 experts its functions in TNBC.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Hua

Deng

et al. 2020

J Exp Clin Cancer Res

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Background: Human ovarian cancer specific transcript 2 (HOST2) is a long non-coding RNA (lncRNA) reported to be specifically high expressed in human ovarian cancer. However, the mechanism that how HOST2 regulates triple negative breast cancer (TNBC) need to be explored. Methods: In this study, expression of HOST2 was determined in 40 TNBC patients and matched non-cancerous tissues by qRT-PCR and in situ hybridization (ISH) assay. The biological functions of HOST2 was measured by losing features. The effect of HOST2 on viability, proliferation and migration was evaluated by MTT, colony formation assay, EDU analysis, transwell invasion assay and nude mouse xenograft model. Fluorescence in situ hybridization (FISH), Luciferase report assay, RNA immunoprecipitation (RIP) assay and Western blot were fulfilled to measure molecular mechanisms. Results: The results showed that HOST2 was up-regulated in BC tissues and cell lines. Clinical outcome analysis demonstrated that high expression of HOST2 was associated with poor prognosis of TNBC patients. Functional experiments illustrated that knockdown of HOST2 significantly suppressed TNBC cell proliferation and migration. Western blot assays, qRT-PCR assays, RIP assays and luciferase reporter assays revealed that HOST2 regulated STAT3 via crosstalk with let-7b. Depression of HOST2 suppressed STAT3-mediated proliferation and migration in TNBC cells. HOST2 could function as a decoy of let-7b to depress expression of STAT3. Conclusions: HOST2 could function as a oncogene and promoted STAT3-mediated proliferation and migration through acting as a competing endogenous RNA, which might act as a potential biomarker for TNBC patients.

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Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Hua

Deng

et al. 2020

J Exp Clin Cancer Res

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show abstract

“…HOST2 is a newly discovered lncRNA, and it was originally found in ovarian cancer [16] and exerted proliferative effects and migration facilitation in ovarian cancer [17]. However, accumulating evidence proposes that HOST2 also plays a part in other cancer cells, such as hepatocellular carcinoma [28], breast cancer [29,30], pancreatic cancer [31], HPV-positive cervical cancer [32] and gastric cancer [33]. Therefore, the functions of HOST2 in cancer cells deserve further research.…”

Section: Discussionmentioning

confidence: 99%

Sinomenine hydrochloride exerts antitumor outcome in ovarian cancer cells by inhibition of long non-coding RNA HOST2 expression

Xu¹,

Jiang²,

Wang³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Accumulating evidence displays that sinomenine hydrochloride (SH) are utilised to treat a variety of cancers. Nevertheless, the influences of SH on ovarian cancer stay blurry. We endeavoured to uncover the antitumor effects of SH on ovarian cancer and underlying mechanism(s). Methods: Human ovarian epithelial cell line (HOEpiC), Caov3 and SKOV3 cells were administrated with SH and/or transfection with pc-long non-coding RNA (lncRNA) human ovarian cancer-specific transcript 2 (HOST2), then cell viability, cell cycle and apoptosis and the related-proteins were respectively inspected by MTT, flow cytometry, and Western blot. In addition, expression of HOST2 was investigated by real-time PCR. Kaplan-Meier manner with the log-rank investigation was achieved to calculate overall survival. Results: SH remarkably repressed cell viability, evoked apoptosis and induced cell cycle arrest in G0/ G1. Moreover, SH statistically decreased HOST2 expression in Caov3 and SKOV3 cells. Overexpression of HOST2 significantly reversed the effects of SH on Caov3 cell viability, cell cycle and apoptosis. Clinical findings confirmed that HOST2 was profoundly higher expressed in ovarian cancer tissues and cells, and HOST2 predicated unfavourable prognosis of ovarian cancer individuals. Conclusion: Our findings recommended that SH exerted the antitumor effect in ovarian cancer cells by hindering expression of HOST2.

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“…a number of studies have demonstrated that lncrnas serve a regulatory role in Gc as oncogenes or tumor suppressor genes (8,9). For example, lncRNA human ovarian cancer specific transcript 2 has been reported to accelerate cell proliferation and metastasis in Gc (10). in addition, Pan et al (11) observed that lncrna differentiation antagonizing non-protein coding rna promoted Gc cell proliferation and invasion by activating spalt-like transcription factor 4. in recent years, lncrna ViM antisense rna 1 (ViM-aS1) has been reported to promote cell migration and invasion through regulating the epithelial-mesenchymal transition (eMT) in colorectal cancer and preeclampsia (12,13).…”

Section: Introductionmentioning

confidence: 99%

lncRNA VIM‑AS1 promotes cell proliferation, metastasis and epithelial‑mesenchymal transition by activating the Wnt/β‑catenin pathway in gastric cancer

Sun

Li²,

Yin³

et al. 2020

Mol Med Rep

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The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding rna ViM antisense rna 1 (ViM-aS1) in gastric cancer (Gc). The expression of ViM-aS1 was analyzed in tissues from patients with Gc and Gc cell lines by reverse transcription-quantitative (rT-q)Pcr. The relationship between ViM-aS1 expression and overall survival time of patients with Gc was also assessed. To determine the biological functions of ViM-aS1, cell counting Kit-8 assay, colony formation assay, flow cytometry, wound healing assay and Transwell assay were employed. The targeting relationship among ViM-aS1, microRNA (miR)-8052 and frizzled 1 (FZD1) was verified by the dual luciferase reporter gene assay. The underlying molecular mechanism of ViM-aS1 on Gc was determined by rT-qPcr and western blotting. in addition, tumor formation was detected in nude mice. The results of the present study demonstrated that ViM-aS1 was highly expressed in Gc tissues and cells. in addition, ViM-aS1 expression was demonstrated to be closely related to the prognosis of patients with Gc. notably, silencing ViM-aS1 inhibited the proliferation, migration and invasion, and enhanced apoptosis of aGS and HGC-27 cells. Silencing VIM-AS1 significantly increased the protein expression levels of cleaved caspase-3, Bax and e-cadherin, but decreased the protein expression levels of Bcl-2, n-cadherin, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, β-catenin, cyclin d1, c-myc and FZd1. additionally, silencing ViM-aS1 inhibited tumor growth in nude mice. cumulatively, the present study demonstrated that ViM-aS1 may promote cell proliferation, migration, invasion and epithelial-mesenchymal transition by regulating FdZ1 and activating the Wnt/β-catenin pathway in Gc.

show abstract

Long non-coding RNA HOST2 enhances proliferation and metastasis in gastric cancer

Cited by 5 publications

References 23 publications

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Sinomenine hydrochloride exerts antitumor outcome in ovarian cancer cells by inhibition of long non-coding RNA HOST2 expression

lncRNA VIM‑AS1 promotes cell proliferation, metastasis and epithelial‑mesenchymal transition by activating the Wnt/β‑catenin pathway in gastric cancer

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