LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

Chen, Si; Li, Weiguo; Ai, Guo

doi:10.1042/bsr20190447

Cited by 24 publications

(26 citation statements)

References 28 publications

(41 reference statements)

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“…LncRNA KCNQ1OT1 restrains the sensitivity of colon cancer cells to oxaliplatin via regulation of miR‐34a/ATG4B pathway . The tumour‐promoting role of LOXL1‐AS1 has been confirmed in multiple cancers, including glioblastoma, cholangiocarcinoma, prostate cancer and osteosarcoma . Nevertheless, the biological function of LOXL1‐AS1 in gastric cancer is still an emerging field to be explored.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

Sun

Фан

et al. 2019

Cell Proliferation

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Objectives As one of the most life‐threatening malignancies, gastric cancer is the third contributor of cancer mortalities globally. Increasing studies have proven the regulatory roles of lncRNAs in the development of diverse malignant tumours. But little is known about its function and molecular mechanism in gastric carcinoma. Materials and methods RT‐qPCR was performed to measure the expression pattern of LOXL1‐AS1 in gastric cancer. To ascertain its definite role, CCK‐8, EdU, Western blot, transwell and sphere formation assays were adopted. RNA pull‐down, RIP, ChIP and luciferase reporter assays were carried out to investigate the molecular mechanism of LOXL1‐AS1 in gastric carcinoma. Results LOXL1‐AS1 was highly expressed in tissues and cells of gastric cancer. The upregulation of LOXL1‐AS1 predicted poor prognosis in gastric carcinoma. Our findings demonstrated that LOXL1‐AS1 accelerated the deterioration of gastric cancer by inducing cell proliferation, migration, EMT and stemness. Moreover, the expression of USF1 in gastric cancer was higher than in normal control and LOXL1‐AS1 negatively modulated USF1. Functionally, LOXL1‐AS1 acted as a ceRNA to upregulate USF1 via sponging miR‐708‐5p. Besides, we confirmed USF1 promoted the transcription of stemness marker SOX2. Rescue experiments testified the stimulative role of LOXL1‐AS1/miR‐708‐5p/USF1 pathway in gastric cancer progression. It was also validated that LOXL1‐AS1 facilitated cell growth of gastric carcinoma in vivo. Conclusions Our study unravelled that LOXL1‐AS1/miR‐708‐5p/USF1 pathway contributed to the development of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

Sun

Фан

et al. 2019

Cell Proliferation

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“…9 TTN-AS1 promoted colorectal cancer proliferation via sponging miR-376a-3p and upregulating KLF15. 10 Small nucleolar RNA host gene 7 (SNHG7), with a length of 2157 bp, is a newly discovered lncRNA which was reported to enhance the progression of a series of cancer types, including pancreatic cancer, 11 lung cancer, 12 bladder cancer, 13 colorectal cancer 14 and esophageal cancer. 15 However, whether SNHG7 also play roles in CC development has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA SNHG7 Functions as an Oncogene in Cervical Cancer by Sponging miR-485-5p to Modulate JUND Expression</p>

Zhao¹,

Zhang²,

Long³

et al. 2020

OTT

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Background: Long non-coding RNA (LncRNA) SNHG7 is involved in the development of multiple cancers. However, its role in cervical cancer (CC) has not been elucidated. This study aimed to explore the function of SNHG7 in CC progression and the underlying mechanisms. Materials and Methods: The expression levels of SNHG7 and miR-485-5p in CC tissues and cell lines were measured by qPCR. Functional experiments including CCK-8 assay, wound healing assay, transwell assay, flow cytometry, Western blot, luciferases reporter assay and immunoprecipitation (RIP) were performed to explore the SNHG7/miR-485-5p/JUND pathway. Additionally, in vivo study was carried out by establishing tumor xenograft models. Results: We found that SNHG7 was markedly enhanced in CC tissues and cell lines, and associated with poor clinical characteristics. In vitro, knockdown of SNHG7 inhibited CC cell proliferation, migration and invasion, as well as aggravated cell apoptosis. As to mechanism investigation, rescue experiments revealed that miR-485-5p inhibitor could partially reverse the effects on CC cells induced by SNHG7 knockdown. SNHG7 upregulated JUND expression via miR-485-5p. Moreover, tumor xenograft models were established to confirm the findings in vivo. Conclusion: SNHG7 promoted CC progression through miR-485-5p/JUND axis. The SNHG7/miR-485-5p/JUND pathway might provide a novel therapeutic target for CC treatment.

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“…As reported previously, LOXL1-AS1 contributes to cell proliferation and metastasis in medulloblastoma through regulating PI3K/AKT signaling [19]. LOXL1-AS1 functions as an oncogene in the progression of osteosarcoma [20]. LOXL1-AS1 contributes to prostate cancer cell growth by regulating miR-541-3p/CCND1 axis [21].…”

Section: Discussionmentioning

confidence: 75%

LOXL1-AS1 contributes to the proliferation and migration of laryngocarcinoma cells through miR-589-5p/TRAF6 axis

Yao

et al. 2020

Cancer Cell Int

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Background LOXL1-AS1 is a long non-coding RNA (lncRNA) that plays crucial roles in various cancers. However, the functional role of LOXL1-AS1 in laryngocarcinoma remains unclear. Thus we planned to probe into the function and underlying mechanism of LOXL1-AS1 in laryngocarcinoma. Methods Gene expression was evaluated in laryngocarcinoma cells using RT-qPCR. The ability of cell proliferation and migration was assessed by CCK8, colony formation, wound healing and transwell assays. The interaction among LOXL1-AS1, miR-589-5p and TRAF6 was detected by Ago2-RIP, RNA pull down and luciferase reporter assays. Results LOXL1-AS1 was overexpressed in laryngocarcinoma cells. Silencing of LOXL1-AS1 suppressed cell proliferation, migration and EMT in laryngocarcinoma. Moreover, miR-589-5p, the downstream of LOXL1-AS1, directly targeted TRAF6 in laryngocarcinoma. Importantly, LOXL1-AS1 augmented TRAF6 expression in laryngocarcinoma cells by sequestering miR-589-5p. Besides, miR-589-5p worked as a tumor-inhibitor while TRAF6 functioned as a tumor-facilitator in laryngocarcinoma. Of note, rescue experiments both in vitro and in vivo validated that LOXL1-AS1 aggravated the malignancy in laryngocarcinoma by targeting miR-589-5p/TRAF6 pathway. Conclusions LOXL1-AS1 promotes the proliferation and migration of laryngocarcinoma cells through absorbing miR-589-5p to upregulate TRAF6 expression.

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LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

Cited by 24 publications

References 28 publications

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

LncRNA LOXL1‐AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR‐708‐5p/USF1 pathway

<p>LncRNA SNHG7 Functions as an Oncogene in Cervical Cancer by Sponging miR-485-5p to Modulate JUND Expression</p>

LOXL1-AS1 contributes to the proliferation and migration of laryngocarcinoma cells through miR-589-5p/TRAF6 axis

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