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. 2019 Oct 30;39(10):BSR20191348.
doi: 10.1042/BSR20191348.

MiR-182 regulates cell proliferation and apoptosis in laryngeal squamous cell carcinoma by targeting the CRR9

Yuan Lv  1 , Dong Ye  1 , Shijie Qiu  1 , Jian Zhang  1 , Zhisen Shen  1 , Yi Shen  1 , Hongxia Deng  1
Affiliations

MiR-182 regulates cell proliferation and apoptosis in laryngeal squamous cell carcinoma by targeting the CRR9

Yuan Lv et al. Biosci Rep. .

Retraction in

Abstract

Background: The effect of miR-182 on the expressions of CRR9 in laryngeal squamous cell carcinoma (LSCC) cells, and the impact on invasion and metastasis of LSCC were investigated in the present paper.

Methods: The expressions of miR-182 in LSCC tissue and cell line were detected by RT-qPCR. MTT assay and Annexin V staining were used to detect the effects of miR-182 on tumor cells proliferation. Target gene prediction and screening, and luciferase reporter assay were designed to verify downstream target genes of miR-182. The mRNA and protein expressions of CRR9 were detected by qRT-PCR and Western blot. Finally, the expressions of CRR9 were measured by transfecting cells with miR-182 in mice.

Results: Compared with normal tissue and cell, the expressions of miR-182 in tumor tissues and cells were much lower. Over-expressions of miR-182 can increase apoptosis rate. Luciferase reporter assay revealed that CRR9 was a downstream gene of miR-182. Reintroduction of CRR9 abolished miR-182-induced LSCC cell growth inhibition. In animal models, over-expressions of miR-182 can reduce tumor weight and promote apoptosis.

Conclusion: miR-182 can inhibit the proliferation of LSCC cells by directly inhibiting the expressions of CRR9, thereby suppressing the occurrences and developments of LSCC.

Keywords: CRR9; apoptosis; laryngeal squamous cell carcinoma; miR-182; proliferation.

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Conflict of interest statement

The study agreed with the Ethics Committee of Li huili hospital affiliated to Ningbo University. Experiments using human materials were performed in strict accordance with Declaration of Helsinki. Informed consent was signed for all patients.

The authors declare there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. The expressions of miR-182 in LSCC samples and cell lines
(A) The level of miR-182 in 30 LSCCs in normal controls and LSCC samples. (B) Expression levels of miR-182 levels in Hep2 cells, TU212 cells, and HaCaT cells. **P<0.01, ***P<0.001.
Figure 2
Figure 2. The expressions of miR-182 induced inhibition, proliferation and apoptosis in LSCC cells
(A) The expressions of miR-182 in LSCC cells transfected with miR-182 mimic or hybrid. (B) Cell viability. (C) Colony formation assay was examined by colony formation assay. (D) Apoptosis was assessed by Annexin V-PI staining. **P<0.01.
Figure 3
Figure 3. CRR9 was a direct target of miR-182
(A) The targeting site and corresponding mutant sequence in the 3′UTR of CRR9. (B) Relative luciferase activity of HEK293 cells after co-transfection with wild-type (WT) or mutant (MUT) CRR9 3′UTR luciferase reporter vector and miR-182 mimic or scramble. qRT-PCR (C) and Western blot (D) analysis of CRR9 expressions. Cell viability (E), cell viability (F) respectively. *P<0.05, **P<0.01.
Figure 4
Figure 4. The expressions of miR-182 in vivo
(A) The images of tumor size (n=6). (B) Tumor growth curve. (C) Measurement of tumor weight. qRT-PCR (D) and Western blot (E) analyses of CRR9 expressions. **P<0.01.
See this image and copyright information in PMC

References

    1. Vaezi M.F., Qadeer M.A., Lopez R.and Colabianchi N. (2006) Laryngeal cancer and gastroesophageal reflux disease: a case-control study. Am. J. Med. 119, 768–776 10.1016/j.amjmed.2006.01.019 - DOI - PubMed
    1. Sawatsubashi M., Yamada T., Fukushima N., Mizokami H., Tokunaga O.and Shin T. (2000) Association of vascular endothelial growth factor and mast cells with angiogenesis in laryngeal squamous cell carcinoma. Virchows Arch. 436, 243–248 10.1007/s004280050037 - DOI - PubMed
    1. Castro M.A.F., Dedivitis R.A.and Ribeiro K.C.B. (2007) Comorbidity measurement in patients with laryngeal squamous cell carcinoma. Oper. Res. Lett. 69, 146–152 - PubMed
    1. Silveira N.J.F., Varuzza L., Machadolima A., Lauretto M.D.S., Pinheiro D.G., Rodrigues R.V. et al. . (2008) Searching for molecular markers in head and neck squamous cell carcinomas (HNSCC) by statistical and bioinformatic analysis of larynx-derived SAGE libraries. BMC Med. Genet. 1, 56 - PMC - PubMed
    1. Maurizi M., Almadori G., Ferrandina G., Distefano M., Romanini M.E., Cadoni G. et al. . (1996) Prognostic significance of epidermal growth factor receptor in laryngeal squamous cell carcinoma. Br. J. Cancer 74, 1253–1257 10.1038/bjc.1996.525 - DOI - PMC - PubMed

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