Correlation of IGF1R expression with ABCG2 and CD44 expressions in human osteosarcoma

Kim, Cheung-Kue; Oh, Sun-Ju; Kim, Sook-Ja; Leem, Sun‐Hee; Heo, Jeonghoon; Chung, So-Hak

doi:10.1007/s13258-017-0639-z

Cited by 13 publications

(14 citation statements)

References 25 publications

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“…IGF-1R is a transmembrane tyrosine kinase receptor of the insulin receptor family and contains two extracellular α subunits and two transmembrane β subunits (45). Numerous studies have reported that IGF-1R is frequently overexpressed in a variety of human cancer types, including gastric cancer (46), breast cancer (47), glioblastoma (48), renal cell carcinoma (49) and osteosarcoma (50). In NSCLC, IGF-1R expression has been revealed to be upregulated, and significantly associated with tumor size, tumor grade and response to chemotherapy (25)(26)(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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MicroRNAs (miRNAs/miRs) are frequently differentially expressed in non-small cell lung cancer (NSCLC), and differential miRNAs expression may be closely associated with NSCLC genesis and development. Therefore, an in-depth investigation of the cancer-associated miRNAs that are crucial for NSCLC pathogenesis may provide effective therapeutic targets for patients with this aggressive malignant tumor type. The expression levels and roles of miR-877 have been well studied in hepatocellular carcinoma and renal cell carcinoma. However, the expression pattern and functions of miR-877 in NSCLC as well as associated underlying mechanisms, to the best of our knowledge, have not yet been investigated. The present study revealed that miR-877 expression was downregulated in NSCLC tissues and cell lines. Low miR-877 expression was significantly associated with TNM stage and distant metastasis in patients with NSCLC. Functional experiments demonstrated that recovery of miR-877 expression restricted the proliferation and invasion of NSCLC cells. In addition, bioinformatics analysis predicted insulin-like growth factor 1 receptor (IGF-1R) as a potential target of miR-877. Luciferase reporter assays, reverse transcription-quantitative PCR and western blot analysis further validated that IGF-1R was a direct target of miR-877 in NSCLC. Furthermore, IGF-1R expression was markedly upregulated in NSCLC tissues, and exhibited an inverse correlation with miR-877 expression. Additionally, IGF-1R overexpression reversed the inhibitory effects in NSCLC cells caused by miR-877 upregulation. These findings demonstrated that miR-877 attenuated NSCLC cell proliferation and invasion, at least partly, by downregulating IGF-1R expression, thereby providing an new candidate biomarker for the diagnosis and therapy of patients with NSCLC.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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“…Of note, we found that ABCG2 expression level was signi cantly increased in patients with decreased disease free survival and poor response to chemotherapy. It was in accordance with previous study reporting that elevated levels of ABCG2 have a vital role in OS prognosis [19]. On the basis of these data, we proposed that ABCG2 may become a promising therapeutic target for OS patients.…”

Section: Discussionsupporting

confidence: 92%

High expression of ABCG2 is associated with doxorubicin resistance of osteosarcoma

Shu¹,

Yuan²,

Huang³

et al. 2020

Preprint

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Objectives Previous studies showed overexpression of ABCG2 in a variety of tumor tissues, which could potentially indicate the probability of chemotherapy resistance. This study aimed to reveal the role of ABCG2 in the development of doxorubicin (DOX) resistance and the prognosis of OS. Methods 68 OS patients were included in this study. Tumor tissues were collected for each patient during surgery. DOX-resistant OS cell lines were induced by consecutive exposure of gradually increasing concentration of DOX to the parental cell lines. Lentivirus was used for the knockdown of ABCG2 in OS cells. Cells were treated with the gradient concentration of DOX and the viability was assessed by CCK8 assay. Total RNA was isolated from the tumor tissues or tumor cells, and the expression of ABCG2 was analyzed by qPCR. The relationship between ABCG2 expression and clinicopathological characteristics of the patients was analyzed using the Student’s t-test or the Chi-square test. Cumulative survival time was calculated by the Kaplan-Meier method and analyzed by the log-rank test. P < 0.05 was considered statistically significant. Results DOX-resistant OS cells were successfully established through continuous exposure to DOX. 48 h after DOX exposure, the IC 50 value of DOX-resistant HOS cells and DOX-resistant U2OS were 3.5 µM and 3.25 µM, respectively. By contrast, those of the untreated HOS and U2OS cells were 1.15 µM and 0.93 µM, respectively (p < 0.01). The mRNA expression level of ABCG2 was significantly increased in DOX-resistant cell lines. The CCK-8 assay showed that the DOX-resistant HOS cells and DOX-resistant U2OS cells transfected with ShABCG2 were more sensitive to the DOX treatment than those transfected with ShCtrl. Analysis of gene expression in OS tissues showed remarkably higher expression of ABCG2 as compared with adjacent normal tissues (p < 0.01). The disease-free survival time of patients with high expression level of ABCG2 had obviously decreased survival time than the patients with low expression (p < 0.01). Conclusions ABCG2 expression level was significantly associated with the resistance to DOX and the overall survival of OS patients. ABCG2 may become a promising therapeutic target for OS patients.

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“…A higher level of CD44 expression in OS tissues is apparent in patients with shorter survival and those with an unfavorable response to neoadjuvant chemotherapy [ 54 ]. Furthermore, CD44 expression is predictive of poor survival, metastasis, recurrence, and drug resistance in patients with OS [ 132 , 133 ].…”

Section: Ecm Components As Prognostic Biomarkers In Osmentioning

confidence: 99%

The role of extracelluar matrix in osteosarcoma progression and metastasis

Cui

Dean

Hornicek

et al. 2020

J Exp Clin Cancer Res

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Osteosarcoma (OS) is the most common primary bone malignancy and responsible for considerable morbidity and mortality due to its high rates of pulmonary metastasis. Although neoadjuvant chemotherapy has improved 5-year survival rates for patients with localized OS from 20% to over 65%, outcomes for those with metastasis remain dismal. In addition, therapeutic regimens have not significantly improved patient outcomes over the past four decades, and metastases remains a primary cause of death and obstacle in curative therapy. These limitations in care have given rise to numerous works focused on mechanisms and novel targets of OS pathogenesis, including tumor niche factors. OS is notable for its hallmark production of rich extracellular matrix (ECM) of osteoid that goes beyond simple physiological growth support. The aberrant signaling and structural components of the ECM are rich promoters of OS development, and very recent works have shown the specific pathogenic phenotypes induced by these macromolecules. Here we summarize the current developments outlining how the ECM contributes to OS progression and metastasis with supporting mechanisms. We also illustrate the potential of tumorigenic ECM elements as prognostic biomarkers and therapeutic targets in the evolving clinical management of OS.

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Correlation of IGF1R expression with ABCG2 and CD44 expressions in human osteosarcoma

Cited by 13 publications

References 25 publications

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

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

High expression of ABCG2 is associated with doxorubicin resistance of osteosarcoma

The role of extracelluar matrix in osteosarcoma progression and metastasis

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