Coexistence of her2, ki67, and p53 in osteosarcoma: A strong prognostic factor

Mardanpour, Keykhosro; Rahbar, Mahtab; Mardanpour, Sourena

doi:10.4103/1947-2714.183013

Cited by 29 publications

(10 citation statements)

References 16 publications

(23 reference statements)

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“…9 Ki67 has been reported to be significantly upregulated in a variety of tumor tissues and cells, such as lung, 10 gastric, 11 colon, 12 ovarian, 13 and OS. 14 Our results are consistent with these reports. Ki67 expression was significantly suppressed by SRPX2 knockdown.…”

Section: Dovepresssupporting

confidence: 94%

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

Wu¹,

Wang²,

Chen³

et al. 2020

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Background/Purpose: Osteosarcoma (OS), a primary bone malignancy, is characterized by a high rate of metastasis. It has been found that Sushi repeat containing protein X-linked 2 (SRPX2) is involved in tumor cell proliferation, adhesion, invasion and migration. The current work aimed to explore the effect of SRPX2 on OS cell invasion and proliferation. Methods: Immunohistochemistry (IHC), Western blotting and reverse transcriptionpolymerase chain reaction (RT-PCR) were used to detect the expression of the associated protein in OS tissues and cell lines. Cell counting kit-8 (CCK8), transwell and colony formation assays were used to determine cell viability, invasion, and proliferation, respectively. The in vivo tumorigenic ability of SRPX2 gene was determined using nude mouse tumorigenesis test. Results: SRPX2 knockdown suppressed the viability, while SRPX2 overexpression increased the invasion and colony formation ability of the cells in vitro. In vivo experiments demonstrated that SRPX2 knockdown inhibited tumor growth and invasion as evidenced by decreased Ki67 and N-cadherin levels, and increased E-cadherin level. Downregulation of SRPX2 increased YAP phosphorylation resulting in reduced nuclear translocation to activate Hippo signaling pathway. The promotion of cell viability, colony-forming ability, and invasion, and the inhibition of CTGF, Cyr61, and Birc5 levels promoted by SRPX2 overexpression were reversed by YAP inhibition. Conclusion: SRPX2 increased cell proliferation and invasion in osteosarcoma by activating Hippo signaling pathway.

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Section: Dovepresssupporting

confidence: 94%

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

Wu¹,

Wang²,

Chen³

et al. 2020

OTT

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“…The tumor volume and weight were smaller in the MCM2 and MCM3 knockdown groups than the scramble group (Figure 4B–4D). As shown in Figure 4E and 4F, based on an immunohistochemical analysis, the levels of the tissue proliferation marker Ki-67 [18] was lower in the sh-MCM2 and sh-MCM3 tumors compared to those in sh-control tumors. Taken together, these results indicated that MCM2 or MCM3 knockdown could hinder the tumorigenesis of osteosarcoma cells in vivo .…”

Section: Resultsmentioning

confidence: 99%

Minichromosome maintenance protein 2 and 3 promote osteosarcoma progression via DHX9 and predict poor patient prognosis

et al. 2017

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A label free quantitative proteomic approach (SWATH™ experiment) was performed to identify tumor-associated nuclear proteins that are differentially expressed between osteosarcoma cells and osteoblast cells. By functional screening, minichromosome maintenance protein 2 (MCM2) and minichromosome maintenance protein 3 (MCM3) were found to be related to osteosarcoma cell growth. Here, we show that knockdown of MCM2 or MCM3 inhibits osteosarcoma growth in vitro and in vivo. In co-immunoprecipitation and co-localization experiments, MCM2 and MCM3 were found to interact with DExH-box helicase 9 (DHX9) in osteosarcoma cells. A rescue study showed that the decreased growth of osteosarcoma cells by MCM2 or MCM3 knockdown was reversed by DHX9 overexpression, indicating that MCM2 and MCM3 activity was DHX9-dependent. In addition, the depletion of DHX9 hindered osteosarcoma cell proliferation. Notably, MCM2 and MCM3 expression levels were positively correlated with the DHX9 expression level in tumor samples and were associated with a poor prognosis in patients with osteosarcoma. Taken together, these results suggest that the MCM2/MCM3–DHX9 axis has an important role in osteosarcoma progression.

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“…Over-expression of MTA-1 has been noted in high-grade osteosarcoma tumor samples with little to no expression in low-grade samples (9). Mardanpour et al evaluated tumor samples from 56 osteosarcoma patients and noted a correlation between increased p53 and Ki67 with worse PFS and OS (18). In 47 resected osteosarcomas following neoadjuvant chemotherapy, increased p53 expression correlated with worse overall survival while expression in biopsy samples was not predictive of chemotherapy response or survival (19).…”

Section: Discussionmentioning

confidence: 99%

Differential Outcomes and Biologic Markers of Radiation-Associated vs. Sporadic Osteosarcoma: A Single-Institution Experience

et al. 2020

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Background: Radiation-associated osteosarcoma (RAO) is a rare, life-threatening complication from radiation. Many physicians presume RAO has a worse prognosis than sporadic osteosarcoma (SO), although limited objective data exist. We conducted a retrospective study comparing these entities. Methods: We identified adults treated at our institution with osteosarcoma (1990-2016) and categorized tumors as SO or RAO based on location within a prior radiation field. We extracted data on demographics, treatment and primary malignancy and examined available tumor samples for MTA-1 and ezrin using immunohistochemistry (IHC). Results: Of 159 identified patients, 28 had RAO, diagnosed at a median interval from radiation of 11.5 years (1.5-28 years). Median follow-up was 2.8 years (0.1-19.6 years). Median progression free survival (PFS) and overall survival (OS) were not significantly different in the small population of patients with metastases, SO (n = 20) vs. RAO (n = 6): PFS 10.3 months vs. 4.8 months (p = 0.45) and OS 15.6 months vs. 6.1 months (p = 0.96), respectively. For the larger group with localized disease, median relapse-free survival (RFS) and OS were significantly different, NR vs. 12.2 months (p < 0.001) and NR vs. 27.6 months (p = 0.001) in SO (n = 111) vs. RAO (n = 22), respectively. On IHC, there were significant differences in distribution of high, intermediate or low MTA-1 (p = 0.015) and ezrin (p = 0.002) between RAO and SO tumors. Conclusions: Patients with metastases at diagnosis fared poorly irrespective of prior radiation. RAO patients with localized disease had worse outcomes without detectable differences in therapy rendered or treatment effect in resected specimens. Higher expression of MTA-1 in RAO patients may suggest an underlying difference in tumor biology to explain differences in outcomes.

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Coexistence of her2, ki67, and p53 in osteosarcoma: A strong prognostic factor

Cited by 29 publications

References 16 publications

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

<p>SRPX2 Promotes Cell Proliferation and Invasion in Osteosarcoma Through Regulating Hippo Signaling Pathway</p>

Minichromosome maintenance protein 2 and 3 promote osteosarcoma progression via DHX9 and predict poor patient prognosis

Differential Outcomes and Biologic Markers of Radiation-Associated vs. Sporadic Osteosarcoma: A Single-Institution Experience

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