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  • 1
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 10, No. 3 ( 2019-03-04)
    Abstract: Accumulating evidence from clinical and epidemiological studies has highlighted the close correlation between the individual risk of cancer and nervous system diseases. The expression of neuronal pentraxin 2 (NPTX2) is absent in Alzheimer’s disease, anxiety, and depression. Herein, we found that NPTX2 mRNA and protein expression was significantly upregulated in colorectal carcinoma (CRC). NPTX2 expression level gradually increased with CRC progression and was closely associated with poor prognosis. In vitro and in vivo studies demonstrated that NPTX2 promoted CRC proliferation and metastasis through the activation of the Wnt/β-catenin signaling pathway. As NPTX2 receptors are absent on CRC cells, NPTX2 was shown to physically interact with frizzled class receptor 6 (FZD6) to promote β-catenin translocation into the cell nucleus, resulting in an increase in the expression of MYC, cyclin D1, snail, and N-cadherin along with a decrease in the expression of E-cadherin. Knockdown of FZD6 expression with a small-interfering RNA almost completely reversed the proliferative effects of NPTX2 on CRC development. In conclusion, NPTX2, a molecule related to nervous system diseases, promotes CRC cell proliferation and metastasis through the activation of the Wnt/β-catenin pathway via direct interaction with FZD6.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2541626-1
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  • 2
    Online Resource
    Online Resource
    Frontiers Media SA ; 2020
    In:  Frontiers in Oncology Vol. 10 ( 2020-11-10)
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 10 ( 2020-11-10)
    Type of Medium: Online Resource
    ISSN: 2234-943X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2649216-7
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  • 3
    In: Journal of Immunology Research, Hindawi Limited, Vol. 2021 ( 2021-3-15), p. 1-12
    Abstract: Mitochondrial Pyruvate Carrier 1 (MPC1), one of the rate-limiting proteins involved in glycolysis metabolism, has been demonstrated as a tumor inhibitor in several cancers. This study was conducted with the aim of exploring the role and underlying mechanisms of MPC2 in colorectal cancer (CRC). Here, we found that MPC2 expression was decreased in CRC samples. According to the analysis on our TMA data, lower expression of MPC2 is correlated with a higher incidence of distant metastasis and lymph node invasion, bigger tumor size, low survival rate of patients, and advanced T stages. Functionally, in vivo/vitro experiments showed that MPC2 knockdown induced CRC cell proliferation and growth, while MPC2 overexpression inhibited the proliferation and growth of CRC. Further study demonstrated that MPC2 knockdown resulted in aerobic glycolysis in CRC cells. Similarly, MPC2 overexpression in CRC cells also caused inhibited aerobic glycolysis. Further study found that MPC2 knockdown in CRC cell lines activated the mTOR signaling pathway, and the addition of rapamycin reversed the promoting effect of MPC2 knockdown on CRC proliferation and glycolysis. Likewise, the addition of MHY1485 also reversed the MPC2 overexpression’s role in hindering aerobic glycolysis in CRC cells. Collectively, our study established that low expression of MPC2 led to CRC growth as well as aerobic glycolysis through the regulation of the mTOR pathway in CRC cells, indicating a potential biomarker and therapy target for CRC.
    Type of Medium: Online Resource
    ISSN: 2314-7156 , 2314-8861
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2817541-4
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2017
    In:  Ophthalmologica Vol. 237, No. 2 ( 2017), p. 85-95
    In: Ophthalmologica, S. Karger AG, Vol. 237, No. 2 ( 2017), p. 85-95
    Abstract: 〈 b 〉 〈 i 〉 Purpose: 〈 /i 〉 〈 /b 〉 To study the effect of autophagy on vitality, migration, and tube formation of RF/6A cells under the condition of 〈 smlcap 〉 D 〈 /smlcap 〉 -glucose. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Cultured RF/6A cells were randomly divided into 4 groups (control, low glucose, high glucose, and high glucose with 3-methyladenine [3-MA]). Autophagy-related proteins (Atg7, p62, and LC3) were monitored. Cell vitality, cell migration, tube formation, reactive oxygen species (ROS) production, and apoptosis were assessed. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Cell vitality significantly decreased and cell migration and tube formation significantly increased in the high-glucose group ( 〈 i 〉 p 〈 /i 〉 〈 0.05). Pretreatment with 3-MA significantly increased cell viability and inhibited cell migration and tube formation ( 〈 i 〉 p 〈 /i 〉 〈 0.05). ROS production increased in the high-glucose group and decreased in the high-glucose with 〈 i 〉 N 〈 /i 〉 -acetylcysteine (NAC) group ( 〈 i 〉 p 〈 /i 〉 〈 0.05). The level of apoptosis increased in the high-glucose group, while it was reduced in the high-glucose with 3-MA group. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Autophagy maybe participates in the formation of retinal neovascularization induced by high glucose.
    Type of Medium: Online Resource
    ISSN: 0030-3755 , 1423-0267
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1483531-9
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  • 5
    In: Oncogene, Springer Science and Business Media LLC, Vol. 42, No. 2 ( 2023-01-05), p. 99-112
    Abstract: The microenvironment of distant organ plays vital roles in regulating tumor metastases. However, little is known about the crosstalk between metastasized tumor cells and target organs. Herein, we found that EFNB2 expression was upregulated in liver metastases (LM) of colorectal cancer (CRC), but not in pulmonary metastases (PM) or primary CRC tumors. EFNB2 played a tumor-promoting role in CRC LM in vitro and in vivo. Through forward signaling, EFNB2-promoted CRC LM by interacting with the EPHB4 receptor. EFNB2/EPHB4 axis enhances LDLR-mediated cholesterol uptake in CRC LM. Subsequently, EFNB2/EPHB4 axis promotes LDLR transcription by regulating STAT3 phosphorylation. Blocking LDLR reversed the role of the EFNB2/EPHB4 axis in promoting CRC LM. Using clinical data, survival analysis revealed that the survival time of patients with CRC LM was decreased in patients with high EFNB2 expression, compared with low EFNB2 expression. Inhibition of the EFNB2/EPHB4 axis markedly prolonged the survival time of BALB/c nude mice with CRC LM with a high cholesterol diet. These findings revealed a key step in the regulation of cholesterol uptake by EFNB2/EPHB4 axis and its tumor-promoting role in CRC LM.
    Type of Medium: Online Resource
    ISSN: 0950-9232 , 1476-5594
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2008404-3
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