MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

Zhou, Guohua; Xie, Jinglian; Gao, Zikun; Yao, Weitao

doi:10.3892/etm.2019.7676

Cited by 11 publications

(11 citation statements)

References 50 publications

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“…Previous studies have reported miR-877-5p expression was distinctly down-regulated and acted as an oncogene in several tumors, including NSCLC. We also provided evidence that miR-877-5p was highly expressed in both NSCLC specimens from our cohort and cell lines, which was consistent with previous ndings 35 . Then, luciferase reporter gene assays assisted in con rming the regulatory role of DNAH17-AS1 in miR-877-5p.…”

Section: Discussionsupporting

confidence: 92%

Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877–5p/CCNA2 pathway

Mao

Jing

2020

Biochemical and Biophysical Research Communications

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Background: A growing number of studies have revealed that long noncoding RNAs (lncRNAs) can function as important oncogenes or tumor suppressors. This study aimed to investigate the regulatory role of lncRNA DNAH17 antisense RNA 1 (DNAH17-AS1) on non-small cell lung cancer (NSCLC) and the underlying molecular mechanisms. Methods: RT-PCR was used to examine the expression of DNAH17-AS1, miR-877-5p and CCNA2 in NSCLC specimens and cell lines. The diagnostic and prognostic values of DNAH17-AS1 expression in NSCLC patients were statistically analyzed. We also evaluated the effects of DNAH17-AS1 on the proliferation, migration, invasion and apoptosis of H1299 and 95D cells. Bioinformatic analysis and luciferase reporter assays were carried to con rm the molecular binding. Results: The expression of DNAH17-AS1 and CCNA2 mRNA was distinctly upregulated in NSCLC specimens and cell lines, while miR-877-5p expression was signi cantly decreased. DNAH17-AS1 could be used to distinguish NSCLC specimens from adjacent non-tumor tissues. Clinical assays revealed that high DNAH17-AS1 was associated with TNM stage, distant metastasis and shorter overall survival and disease-free survival. Functional assays indicated that knockdown of DNAH17-AS1 suppressed the proliferation, migration and invasion of H1299 and 95D cells, and promoted apoptosis. Mechanically, DNAH17-AS1 served as competing endogenous RNA (ceRNA) for miR-877-5p to positively recover CCNA2. Conclusion: We identi ed a novel NSCLC-related lncRNA, DNAH17-AS1 which may exert an oncogenic function via serving as a sponge for miR-877-5p to upregulate CCNA2. Our study presents novel insights into NSCLC progression and provided a prospective therapeutic target for NSCLC.

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Section: Discussionsupporting

confidence: 92%

Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877–5p/CCNA2 pathway

Mao

Jing

2020

Biochemical and Biophysical Research Communications

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“…Consistent with our results, the expression of miR-877-5p in non-small cell lung cancer and colorectal cancer was also reduced. 22,23 Functionally, miR-877-5p has been proposed to suppress cell growth, migration and invasion in hepatocellular carcinoma. 24 These findings indicate that miR-877-5p acts as a tumor suppressor in LSCC.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG16 Promotes the Progression of Laryngeal Squamous Cell Carcinoma by Mediating miR-877-5p/FOXP4 Axis</p>

Wang¹,

Li²,

Zhao³

et al. 2020

OTT

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Objective: Laryngeal cancer is a common malignant tumor in the ENT, of which laryngeal squamous cell carcinoma (LSCC) accounts for more than 90% of laryngeal cancer. The purpose of this study is to investigate the regulatory mechanism of lncRNA SNHG16 in LSCC. Materials and Methods: Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to measure mRNA expression. Cell Counting Kit (CCK-8), Transwell and luciferase reporter assays, flow cytometric analysis and Western blot analysis were used to investigate the function of lncRNA SNHG16 in LSCC. Results: SNHG16 expression was increased in LSCC tissues and cells. The abnormal expression of SNHG16 was associated with clinical stage and lymph node metastasis in LSCC patients. In addition, knockdown of SNHG16 restrained cell proliferation, migration and invasion in LSCC. More importantly, SNHG16 acted as a competitive endogenous RNA in LSCC and regulated FOXP4 expression by making miR-877-5p sponge. Further, SNHG16 promoted LSCC progression by interacting with miR-877-5p and FOXP4. Conclusion: LncRNA SNHG16 promotes the progression of LSCC by sponging miR-877-5p and upregulating FOXP4.

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“…In non-small cell lung cancer (NSCLC), miR-877 is down-regulated, and the recovery of its expression inhibits the proliferation and invasion of NSCLC cells in vitro [23]. In colorectal cancer, the overexpression of miR-877 attenuates the migration, invasion and proliferation of cancer cells, and also inhibits the tumor growth in vivo [24].…”

Section: Discussionmentioning

confidence: 99%

miR-877 inhibits the proliferation, migration, and invasion of osteosarcoma cells by targeting gamma-glutamylcyclotransferase

Jia

Wang

et al. 2021

Endocr J

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Gamma-glutamylcyclotransferase (GGCT) can promote the progression of osteosarcoma (OS). MicroRNAs also play significant roles in regulating the progression of OS. This study was designed to investigate whether miR-877 exerts its function in OS by targeting GGCT. The proliferation of OS cells (Saos-2 and U2OS) was detected by MTT and colony formation assays. The migration and invasion of OS cells were detected by transwell assays. The expressions of miRNAs and GGCT were detected by quantitative real-time PCR and Western blot. The luciferase reporter assay was performed to assess whether miR-877 could target GGCT. miR-877 was down-regulated both in OS tissues and OS cell lines (Saos-2 and U2OS). The overexpression of miR-877 inhibited the proliferation, migration, and invasion of OS cell lines, while the knockdown of miR-877 could negate effects. The expression of GGCT was increased in Saos-2 and U2OS cells. miR-877 could target GGCT, and the mRNA level of GGCT in Saos-2 and U2OS cells was decreased by the overexpression of miR-877. miR-877 overexpression inhibited the migration and invasion and suppressed the proliferation of Saos-2 and U2OS cells, and the overexpression of GGCT reversed this effects. The knockdown of miR-877 promoted the migration and invasion and facilitated the proliferation of Saos-2 and U2OS cells, and the silence of GGCT abolished this effects. Our findings suggested that miR-877 could inhibit the proliferation, migration, and invasion of OS cells by targeting GGCT.

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MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

Cited by 11 publications

References 50 publications

Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877–5p/CCNA2 pathway

Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877–5p/CCNA2 pathway

<p>LncRNA SNHG16 Promotes the Progression of Laryngeal Squamous Cell Carcinoma by Mediating miR-877-5p/FOXP4 Axis</p>

miR-877 inhibits the proliferation, migration, and invasion of osteosarcoma cells by targeting gamma-glutamylcyclotransferase

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