MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan, Xiaojie; Jiang, Lihua; Wu, Xia; Feng, Wen; Lin, Qingfang

doi:10.3892/ijmm.2019.4203

Cited by 11 publications

(22 citation statements)

References 41 publications

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“…MicroRNA (miRNA) is a class of small noncoding RNA, containing 18 to 25 nucleotides that specifically binds to the target gene 3′-untranslated region (3′-UTR) to cause translation inhibition or messenger RNA (mRNA) degradation, thus regulating in gene expression. 27 , 28 The abnormal expression of miRNA is closely related to cell differentiation, stress response, proliferation, apoptosis, and other biological behaviors, thus wielding its impact on the tumorigenesis and progression of diverse cancers. 29 - 31 Accumulating evidences have verified that miR-200 family members, including miR-200a, miR-200b, and miR-200c, exert an antitumor role in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Niu

Huang

et al. 2020

Technol Cancer Res Treat

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Background: PTPRG antisense RNA 1 has been well-documented to exert an oncogenic role in diverse neoplasms. However, the precise role of PTPRG antisense RNA 1 in regulating radiosensitivity of nonsmall cell lung cancer cells remains largely elusive. Methods: Expression levels of PTPRG antisense RNA 1 and miR-200c-3p in nonsmall cell lung cancer tissues and cells were detected by quantitative real-time polymerase chain reaction, while transcription factor 4 expression was examined by immunohistochemistry and Western blot. After nonsmall cell lung cancer cells were exposed to X-ray with different doses in vitro, Cell Counting Kit -8 assay and colony formation assay were conducted to determine the influence of PTPRG antisense RNA 1 on cell viability. Interaction between miR-200c-3p and PTPRG antisense RNA 1 as well as transcription factor 4 was investigated by dual luciferase reporter assay. Result: In nonsmall cell lung cancer tissues, the expressions of PTPRG antisense RNA 1 and transcription factor 4 were significantly upregulated, whereas the expression of miR-200c-3p was downregulated. It was also proved that PTPRG antisense RNA 1 and 3′-untranslated region of transcription factor 4 can bind to miR-200c-3p. Under X-ray irradiation, overexpressed PTPRG antisense RNA 1 could promote the viability and enhance the radioresistance of nonsmall cell lung cancer cells, and this effect was partially weakened by miR-200c-3p mimics. Transcription factor 4 was identified as a target gene of miR-200c-3p, which could be positively regulated by PTPRG antisense RNA 1. Conclusion: PTPRG antisense RNA 1 reduces the radiosensitivity of nonsmall cell lung cancer cells via modulating miR-200c-3p/TCF4 axis.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Niu

Huang

et al. 2020

Technol Cancer Res Treat

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“…Increasing evidence indicates that several types of miRNAs, such as miR-675-5p, miR-361-3p, miR-4286, miR-150-5p miR-625 and miR-4319 play crucial roles in NSCLC regulation (33)(34)(35)(36)(37)(38). miR-208 is highly expressed in cardiac tissue and is dysregulated in several types of cardiovascular diseases (26)(27)(28)(29)(30), such as cardiac ischemia reperfusion injury (24) and acute myocardial infarction (25).…”

Section: Discussionmentioning

confidence: 99%

miR‑208b‑5p inhibits invasion of non‑small cell lung cancer through the STAT3 pathway by targeting interleukin‑9

Tong

Lin

et al. 2020

Oncol Lett

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Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progression. A total of 62 pairs of primary tumor and adjacent normal tissues were collected from patients with NSCLC. miR-208b-5p expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-208b-5p mimics was transfected into NSCLC A549 and H1299 cells in order to upregulate miR-208b-5p expression. Dual-luciferase reporter assay was utilized to investigate the associations between miR-208b-5p and IL9 mRNA. The results demonstrated that miR-208b-5p expression decreased in NSCLC tissues and cell lines. Furthermore, miR-208b-5p overexpression inhibited A549 and H1299 cell proliferation and invasiveness. miR-208b-5p was demonstrated to bind directly to the 3' untranslated region of interleukin-9 (IL-9) and therefore decreased its expression. In the NSCLC-derived cell lines, miR-208b-5p inactivated IL-9/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Furthermore, enhanced IL-9 level decreased the miR-208b-5p-mediated suppression of epithelial-mesenchymal transition in NSCLC cells by inactivating the STAT3 signaling pathway. In conclusion, the findings from this study demonstrated that miR-208b-5p inhibited migration and invasion of NSCLC cells. The anti-tumor activity of miR-208b-5p may be mediated by IL-9 and STAT-3 pathway.

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“…The Wnt/β-catenin signaling pathway has been implicated in a wide range of physiological and pathophysiological cancer processes, including lung cancer [25][26][27][28][29]. Tan et al found that the expression of miR-625 inhibited the proliferation, apoptosis, migration, and invasion in vitro by directly targeting homeobox B5 and deactivating the Wnt/β-catenin pathway [30]. Gao et al confirmed that miRNA-378 promoted the progression of lung cancer by inactivation of Wnt/β-catenin and ERK1/2 pathways [31].…”

Section: Introductionmentioning

confidence: 99%

“…Tan et al . found that the expression of miR-625 inhibited the proliferation, apoptosis, migration, and invasion in vitro by directly targeting homeobox B5 and deactivating the Wnt/β-catenin pathway [ 30 ]. Gao et al .…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

Yan

Deng

2020

Open Life Sciences

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AbstractSevoflurane was frequently used as a volatile anesthetic in cancer surgery. However, the potential mechanism of sevoflurane on lung cancer remains largely unclear. In this study, lung cancer cell lines (H446 and H1975) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assessment and colony formation assay were performed to detect the cell viability and proliferation, separately. Also, transwell assay or flow cytometry assay was applied as well to evaluate the invasive ability or apoptosis in lung cancer cells, respectively. Western blot assay was employed to detect the protein levels of β-catenin and Wnt5a. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of prostate cancer-associated transcript 6 (PCAT6) and miR-326 in lung cancer tissues and cells. The target interaction between miR-326 and PCAT6 or Wnt5a was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. Sevoflurane inhibited the abilities on viability, proliferation, invasion, and activation of Wnt/β-catenin signaling, but promoted apoptosis of H446 and H1975 cells in a dose-dependent manner. The expression of PCAT6 was increased in lung cancer tissues and cells, except for that of miR-326. Besides, sevoflurane could lead to expressed limitation of PCAT6 or improvement of miR-326. This process presented a stepwise manner. Up-regulation of PCAT6 restored the suppression of sevoflurane on abilities of proliferation, invasion, rather than apoptosis, and re-activated the Wnt5a/β-catenin signaling in cells. Moreover, the putative binding sites between miR-326 and PCTA6 or Wnt5a were predicted by starBase v2.0 software online. PCAT6 suppressing effects on cells could be reversed by pre-treatment with miR-326 vector. The promotion of Wnt5a inverted effects led from miR-326 or sevoflurane. Our study indicated that sevoflurane inhibited the proliferation, and invasion, but enhanced the apoptosis in lung cancer cells by regulating the lncRNA PCAT6/miR-326/Wnt5a/β-catenin axis.

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MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Cited by 11 publications

References 41 publications

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

miR‑208b‑5p inhibits invasion of non‑small cell lung cancer through the STAT3 pathway by targeting interleukin‑9

Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

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