MicroRNA‑22 inhibits the proliferation and migration, and increases the cisplatin sensitivity, of osteosarcoma cells

Zhou, Xiang; Natino, Dimple; Xu, Zeng‐Guang; Gao, Zhongyang; He, Xijing

doi:10.3892/mmr.2018.8790

Cited by 19 publications

(19 citation statements)

References 31 publications

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“…17 In osteosarcoma, miR-22 inhibits biological functions and increases cisplatin sensitivity via targeting S100A11. 18 Here, we examined the function of miR-22 in CRC and found that it had a tumorinhibiting role, consistent with the results of other studies. We also showed that miR-22 repressed CRC cell proliferation, migration, and invasion in vitro and in vivo.…”

Section: Discussionsupporting

confidence: 90%

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<p>miR-22 Suppresses Tumor Invasion and Metastasis in Colorectal Cancer by Targeting NLRP3</p>

Cong¹,

Ju²,

Yang³

et al. 2020

CMAR

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This study aimed to investigate the effects of microRNA (miR)-22 on biological behaviors of colon cancer cells and to explore the relationship between miR-22 and NLRP3. Materials and Methods: First, human colon cancer HCT116 cells were transfected with a miR-22 mimic, miR-22 inhibitor, control mimic, and control inhibitor, respectively. CCK8, colony formation, and transwell assays were performed to observe cell proliferation, migration, and invasion. Western blotting was used to analyze the expression of recombinant NLRP3 (NLR family, pyrin domain-containing protein 3) and epithelial-mesenchymal transformation (EMT)-related proteins. The target relationship between miR-22 and NLRP3 was verified by double luciferase report. Second, an NLRP3 inhibitor and NLRP3 mimic were transfected into HCT116 cells, and the biological behaviors and EMT-related proteins were again observed. Finally, a nude mouse xenograft model was constructed to verify the above results. Results: In vitro, compared with the control group, administration of the miR-22 mimic significantly decreased proliferation, migration, and invasion of HCT116 cells, whereas the miR-22 inhibitor markedly increased their proliferation and invasion (p<0.05). Levels of NLRP3, interleukin-1β (IL-1β), matrix metalloproteinase-9 (MMP-9), MMP-2, N-cadherin, and vimentin were significantly reduced after miR-22 mimic transfection (p<0.05). Furthermore, silencing of NLRP3, a downstream gene of miR-22 in HCT116 cells, suppressed proliferation, migration, and invasion of HCT116 cells. However, overexpression of NLRP3 weakened the effects of the miR-22 mimic. In vivo, overexpression of miR-22 slowed the growth rate of tumors and reduced Ki-67 expression in tumor tissues compared with the model group (p<0.05). In tumor tissues, overexpression of miR-22 also decreased expression of NLRP3, IL-1β, MMP-9, MMP-2, N-cadherin, and vimentin compared with the model group (p<0.05). Overexpression of NLRP3 weakened the role of miR-22 overexpression in vivo. Conclusion: miR-22 suppresses cell proliferation, migration, and invasion in colorectal cancer by targeting NLRP3.

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Section: Discussionsupporting

confidence: 90%

“…Previous studies have reported potential functions of miR-22 in various cancers, including CRC 17 and osteosarcoma. 18 In CRC, miR-22 suppresses cell proliferation and migration in vitro and in vivo by targeting HuR. 17 In osteosarcoma, miR-22 inhibits biological functions and increases cisplatin sensitivity via targeting S100A11.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-22 Suppresses Tumor Invasion and Metastasis in Colorectal Cancer by Targeting NLRP3</p>

Cong¹,

Ju²,

Yang³

et al. 2020

CMAR

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“…Previous research has demonstrated that MiR‐22 functions as a tumor suppressor in different malignancies, such as prostatic, breast, and gastric cancers. Furthermore, miR‐22 was appreciably decreased in OS patients while its overexpression could suppress MG‐63 cells from dividing and metastasizing. However, the role of miR‐22 and the underlying mechanism in regulating OS and chemoresistance are hitherto unknown.…”

Section: Introductionmentioning

confidence: 99%

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

Wang

Zhao

Guo

et al. 2019

Orthopaedic Surgery

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Objective To analyze the effect of microRNA‐22 on autophagy and proliferation and to investigate the underlying molecular mechanism of osteosarcoma cell chemotherapy sensitivity. Methods MG‐63 cells were divided into four groups, including a control group, a negative control (NC) group, a cisplatin group, and a cisplatin + miR‐22 group. Proliferation of MG‐63 cells that had been treated with cisplatin and transfected with miR‐22 mimics was determined using MTT assay and colony formation assay. We assessed the degree of autophagy using flow cytometry through cellular staining of the autophagy lysosomal marker monodansylcadaverine (MDC). The effect of microRNA‐22 on autophagy was observed along with the expression levels of Beclin1, LC3, metadherin (MTDH) and ATG5 by western blot and quantitative reverse transcription polymerase chain reaction (qRT‐PCR). Luciferase reporter assay revealed the targeted binding site between miR‐22 and the 3′‐untranslated region (3′‐UTR) of MTDH mRNA. Western blot and qRT‐PCR were used to explore the level of MTDH in the control group, the NC group, the cisplatin group, and the miR‐22 group for 6, 12, and 24 h. Results In the in vitro study, the MTT results indicated that the MG‐63 cells with overexpression of miR‐22 exhibited a significant decline in the proliferation capacity compared with the control group (0.513 ± 0.001, P < 0.0005). Similar to the MTT results, MG‐63 cells that were transfected with miR‐22 mimic (101.0 ± 10.58) formed fewer colonies compared with the cisplatin group (129.7 ± 4.163). MDC staining revealed that miR‐22‐overexpressing osteosarcoma (OS) cells treated with cisplatin showed a significant decrease in the expression of autophagy (7.747 ± 0.117, P < 0.0001). Our data revealed that miR‐22 could regulate not only autophagy but also proliferation in the chemosensitivity of osteosarcoma cells. We found that miR‐22 sensitized osteosarcoma cells to cisplatin treatment by regulating autophagy‐related genes. In addition, Luciferase Reporter Assay revealed that miR‐22 negatively regulated autophagy through direct targeting of MTDH. We performed western blot analysis to detect the MTDH expression level. The results revealed that the overexpression of miR‐22 obviously decreased the expression of MTDH (1.081 ± 0.023, P < 0.001). Conclusion Inhibition of miR‐22 ameliorated the anticancer drug‐induced cell proliferation decrease in osteosarcoma cells. MTDH was identified as the miR‐22 target in OS cells and MTDH‐triggered autophagy played a key function in the miR‐22‐associated chemotherapy sensitivity.

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“…A study uncovers that miR-630 inhibits OS cell proliferation, which may offer a new mechanism underlying the initiation and progression of OS [28]. Similarly, another study scheduled by Zhou, X et al demonstrates that miR-22 may be a promising therapeutic target and a part of a combination treatment alongside chemotherapeutic agents for OS [29]. Our results unveiled that low expression of miR-455-3p was associated with a poor survival rate of patients, indicating the miR-455-3p might function as tumor suppressor in OS.…”

Section: Discussionmentioning

confidence: 98%

MiR-455-3p downregulation facilitates cell proliferation and invasion and predicts poor prognosis of osteosarcoma

2020

J Orthop Surg Res

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Background Osteosarcoma (OS) is one of the most primary malignant bone tumors, mainly attracting children and young adults. The microRNAs are mentioned to play vital roles in many cancers, including OS. The purpose of this study was to explore the expression and function of miR-455-3p in OS and predict the potential effects in clinical diagnosis and prognosis. Method We conducted quantitative real-time PCR to assess the expression of miR-455-3p in OS tissues and cell lines. The Cell Counting Kit-8 assay, Transwell assay, and flow cytometry were performed to assess the ability of miR-455-3p on cell proliferation, migration, invasion, and apoptosis. Kaplan–Meier curve and Cox regression analysis were used to demonstrate the survival outcome. Results This study revealed that the expression of miR-455-3p was decreased in OS tissues and cell lines. The dysregulation of miR-455-3p was in association with tumor size, distant metastasis, and clinical stage. Patients with high miR-455-3p expression had a satisfying survival rate. Multivariate Cox analysis indicated that miR-455-3p was a promising prognostic indicator. Expression of miR-455-3p could inhibit the proliferation, migration, and invasion, and facilitate apoptosis of OS cells in vitro. Conclusion These results indicated the miR-455-3p was a potential clinical therapeutic target and prognostic biomarker by suppressing the proliferation, migration, and invasion, as well as enhancing cell apoptosis.

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MicroRNA‑22 inhibits the proliferation and migration, and increases the cisplatin sensitivity, of osteosarcoma cells

Cited by 19 publications

References 31 publications

<p>miR-22 Suppresses Tumor Invasion and Metastasis in Colorectal Cancer by Targeting NLRP3</p>

<p>miR-22 Suppresses Tumor Invasion and Metastasis in Colorectal Cancer by Targeting NLRP3</p>

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

MiR-455-3p downregulation facilitates cell proliferation and invasion and predicts poor prognosis of osteosarcoma

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