Diagnostic investigations of PLA2G16 and CDH11 expression levels as independent prognostic markers of human osteosarcoma

Azarsina, Salman; Otoukesh, Babak; Taheriazam, Afshin; Kaghazian, Maria; Boddouhi, Bahram; Yahaghi, Emad; Kaghazian, Peyman

doi:10.5114/aoms.2016.59710

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…Increasing evidence has revealed that CDH11 plays a momentous role in the development of a broad series of human malignancies, and identified CDH11 as a functional tumour suppressor which is commonly silenced by promoter methylation 3. Previous studies have shown that CDH11 inhibits invasion and proliferation in head and neck cancer,21 osteosarcoma,8,22 glioma,23 melanoma24 and bladder cancer 25. The correlation between the function of CDH11 and related mechanisms in colorectal cancer remained unclear.…”

Section: Discussionmentioning

confidence: 99%

Cadherin-11 is inactivated due to promoter methylation and functions in colorectal cancer as a tumour suppressor

Yuan¹,

Li²,

Xiang³

et al. 2019

CMAR

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Background: The cadherin-11 ( CDH11 , OB-cadherin) gene is a member of the cadherin family and is located on chromosome 16q22.1. Previous studies have revealed that cadherins play significant roles in the development of many human malignancies. Increasing evidence has identified CDH11 as a functional tumour suppressor, which is commonly silenced by promoter methylation, but the functions of this gene in colorectal cancer (CRC) have been unclear. Methods: The CDH11 expression in primary CRC tissues and cell lines was investigated by qRT-PCR, RT-PCR and immunohistochemistry. The promoter methylation status of CDH11 was measured by methylation-specific PCR (MSP). Cell proliferation assay, colony formation assay, flow cytometry analysis, wound-healing assay, transwell assay and in vivo experiments were used to investigate the function of CDH11 in CRC. The mechanisms of CDH11 also were explored by western blots. Results: Our study suggests that CDH11 downregulation in CRC due to its promoter methylation and induced cell cycle arrest in G0/G1 phase and apoptosis, suppressing tumor cell proliferation, colony formation, migration and invasion by affecting the NF-kB signaling pathway. Conclusion: Overall, CDH11 may be considered as a functional tumour suppressor gene (TSG) in CRC, CDH11 has the potential to serve as a valuable prognostic marker for colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Cadherin-11 is inactivated due to promoter methylation and functions in colorectal cancer as a tumour suppressor

Yuan¹,

Li²,

Xiang³

et al. 2019

CMAR

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“…Despite aggressive treatment, about a third of affected patients die of their disease. More recently [1], many novel targets have been identified and serve as independent prognostic markers of human osteosarcoma. Neoadjuvant chemotherapy followed by surgical resection and additional adjuvant chemotherapy are routine treatment of osteosarcoma and the 5-year-survival rate of patients is 60–70% [2].…”

Section: Introductionmentioning

confidence: 99%

Trichostatin A activates FOXO1 and induces autophagy in osteosarcoma

Bai¹,

Chen²,

Chen³

et al. 2019

aoms

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A b s t r a c tIntroduction: Histone deacetylase inhibitors (HDACIs) inhibit human osteosarcoma growth and cause apoptosis. Previously, we reported that HDACIs induce autophagy via the FOXO1 pathway. Whether there is involvement of autophagy in anti-osteosarcoma activity of HDACIs is still unknown. Material and methods: Confocal microscopy was performed to determine the formation of GFP-LC3 puncta. Western blotting was conducted to measure FOXO1, and autophagy-related protein levels. Small interference RNA (siRNA) specific for FOXO1 was transfected into U2OS cells to knock down FOXO1 expression level. Flow cytometry was performed to quantify cell death. Results: In this study, we first observed that trichostatin A (TSA) induces autophagy in human osteosarcoma cells. Moreover, we found that TSA treatment inhibits the mammalian target of rapamycin (mTOR) signaling pathway and enhances forkhead box O1 (FOXO1) transcriptional activity, which is responsible for the increased autophagy level, while suppression of FOXO1 function by siRNA knockdown markedly decreases TSA-induced autophagy. Conclusions: We found that inhibition of autophagy, either by autophagy inhibitors or ATG gene knockdown, markedly enhances TSA-caused cell death. Taken together, our studies reveal the function of autophagy in HDACI-caused osteosarcoma cell death and thus support the development of a novel therapeutic strategy by combining HDACIs and autophagy inhibitors in osteosarcoma treatment.

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“…Numerous studies have shown a significant downregulation of CDH11 expression in osteosarcoma tissues, and its expression level is notably correlated with patient survival rate. This suggests that CDH11 is likely an independent prognostic factor associated with poorer overall survival in osteosarcoma patients [ [59] , [60] , [61] ].…”

Section: Tumormentioning

confidence: 99%

Cdh11: Roles in different diseases and potential value in disease diagnosis and treatment

Zhang,

Wang,

Zhang

2023

Biochemistry and Biophysics Reports

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Diagnostic investigations of PLA2G16 and CDH11 expression levels as independent prognostic markers of human osteosarcoma

Cited by 6 publications

References 21 publications

<p><em>Cadherin-11</em> is inactivated due to promoter methylation and functions in colorectal cancer as a tumour suppressor</p>

<p><em>Cadherin-11</em> is inactivated due to promoter methylation and functions in colorectal cancer as a tumour suppressor</p>

Trichostatin A activates FOXO1 and induces autophagy in osteosarcoma

Cdh11: Roles in different diseases and potential value in disease diagnosis and treatment

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