<scp>LPLUNC1</scp> reduces glycolysis in nasopharyngeal carcinoma cells through the <scp>PHB1</scp>‐p53/<scp>c‐Myc</scp> axis

Oyang, Linda; Ouyang, Liang; Yang, Lixia; Lin, Jinguan; Xia, Longzheng; Tan, Shiming; Wu, Nayiyuan; Han, Yaqian; Yang, Yiqing; Li, Jian; Chen, Xiaohui; Tang, Yue; Su, Min; Luo, Xin; Li, Jinyun; Wang, Xiong; Zeng, Zhaoyang; Liao, Qianjin; Zhou, Yujuan

doi:10.1111/cas.15662

Cited by 4 publications

(3 citation statements)

References 64 publications

(191 reference statements)

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“…However, the roles of the ARHGAP44 / p53 and C-Myc / Cyclin D1 pathways in osteosarcoma remain unclear. The present study revealed that C-myc and Cyclin D1 may be inhibited by the downregulation of ARHGAP44 and upregulation of p53 expression levels, which is consistent with the findings of Oyang and Yenmis et al [ 33 , 34 ]. These results suggest that the downregulation of ARHGAP44 expression may inhibit the proliferation, invasion, and migration of osteosarcoma tumor cells through the p53 / C-myc / Cyclin D1 pathway (Fig.…”

Section: Discussionsupporting

confidence: 93%

“…There is also a regulatory relationship between p53 , C-myc , and Cyclin D1 . Oyang et al [ 33 ] found that LPLUNC1 reduces the proliferation of nasopharyngeal carcinoma tumor cells through the p53 / C-myc pathway. In breast cancer, metformin reduces the expression of Cyclin D1 by upregulating the p53 expression, thereby promoting tumor apoptosis [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

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ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells

Li,

Xue,

Zhang

et al. 2023

J Orthop Surg Res

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Objective Osteosarcoma is a rare primary malignant tumor of the bone characterized by poor survival rates, owing to its unclear pathogenesis. Rho GTPase-activating protein 44 (ARHGAP44), which belongs to the Rho GTPase-activating protein family, has promising applications in the targeted therapy of tumors. Therefore, this study aimed to investigate the biological function of ARHGAP44 in osteosarcoma and its possible application as a therapeutic target. Methods The expression level of ARHGAP44 in osteosarcoma and its relationship with tumor prognosis were detected using Gene Expression Omnibus database analysis and immunohistochemical staining of clinical specimens. The cell model of ARHGAP44 knockdown was constructed, and the effects of this gene on the malignant biological behavior of osteosarcoma cells were investigated using CCK-8, clone formation, transwell invasion, wound healing, and flow cytometry assays. Western blotting was performed to detect the expression of ARHGAP44, p53, C-myc, and Cyclin D1 in osteosarcoma. Results Biogenic analysis showed that ARHGAP44 was highly expressed in osteosarcoma. This result was associated with poor tumor prognosis and negatively correlated with the expression of the tumor suppressor gene p53. Immunohistochemistry and western blotting revealed significantly upregulated expression of ARHGAP44 in osteosarcoma tissues. Additionally, Kaplan–Meier analysis of clinical specimens suggested that ARHGAP44 was negatively correlated with tumor prognosis. CCK-8, clone formation, transwell invasion, wound healing, and flow cytometry assays showed that downregulation of ARHGAP44 expression significantly reduced the malignant biological behavior of osteosarcoma cells. Furthermore, western blotting showed that the expression level of p53 in osteosarcoma cells was significantly increased after the downregulation of ARHGAP44 expression, whereas the expression of C-myc and Cyclin D1 was significantly decreased compared with that in the control group. Conclusion ARHGAP44 was highly expressed in osteosarcoma and was negatively correlated with its prognosis. The downregulation of ARHGAP44 expression reduced the malignant biological behavior of osteosarcoma cells. These findings suggest that the downregulation of ARHGAP44 expression inhibits the malignant progression of osteosarcoma by regulating the p53/C-myc/Cyclin D1 pathway, demonstrating the potential of ARHGAP44 as a therapeutic target for osteosarcoma.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells

Li,

Xue,

Zhang

et al. 2023

J Orthop Surg Res

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“…5 C, TOM40 knockdown decreased the levels of phosphorylated AKT, mTOR, p70S6K, pS6 and 4E-BP1, suggesting inactivation of the AKT/mTOR signaling pathway. The p53/p21 pathway acts downstream of ROS signaling in NPC cells and is known to trigger apoptosis [ 16 , 22 ]. We found that inhibition of TOM40 increased p21 and p53 levels, along with that of cleaved PARP and cleaved caspase 3, which lie downstream of p53 signaling.…”

Section: Resultsmentioning

confidence: 99%

TOM40 regulates the progression of nasopharyngeal carcinoma through ROS-mediated AKT/mTOR and p53 signaling

Ran,

Zhang,

Zeng

et al. 2023

Discov Onc

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Nasopharyngeal carcinoma (NPC) is a prevalent cancer in Southern China, North Africa, and Southeast Asia. The translocase of the outer membrane (TOM) 40 is a transporter of mitochondrial proteins, and is involved in ovarian cancer cell growth. However, its role in the progression of NPC is still unclear. We found that TOM40 levels were upregulated in NPC tissues and multiple NPC cell lines. In addition, high TOM40 expression in the tumor tissues was associated with poor overall survival and disease specific survival. TOM40 knockdown in the NPC cell lines inhibited their proliferation in vitro and in vivo. Furthermore, TOM40 silencing also increased intracellular production of reactive oxygen species (ROS) and decreased mitochondrial membrane potential (MMP). Mechanistically, the anti-tumor effects of TOM40 silencing were dependent on the inhibition of AKT/mTOR signaling and activation of p53 signaling. To summarize, TOM40 mediates NPC progression through ROS-mediated AKT/mTOR and p53 signaling. Our findings highlight the potential of TOM40 as a therapeutic target for NPC.

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LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1‐p53/c‐Myc axis

et al. 2022

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Cancer cells usually prefer glycolysis to support their proliferation. Our previous studies have shown that the long palate, lung, and nasal epithelial cell clone 1 (LPLUNC1) can up-regulate prohibitin 1 (PHB1) expression to inhibit the proliferation of nasopharyngeal carcinoma (NPC) cells. Given that PHB1 is an important regulator of cell energy metabolism, we explored whether and how LPLUNC1 regulated glucose glycolysis in NPC cells. LPLUNC1 or PHB1 over-expression decreased glycolysis and increased oxidative phosphorylation (OXPHOS)-related protein expression in NPC cells, accompanied by enhancing PHB1 and 14-3-3σ expression and promoting phosphorylated PHB1 nuclear translocation. Coimmunoprecipitation indicated that 14-3-3σ directly interacted with phosphorylated PHB1. PHB1 Y259A mutant over-expression abrogated the decreasing glycolysis and increasing OXPHOS-related protein expression induced by LPLUNC1 over-expression in NPC cells. LPLUNC1 over-expression also increased p53, but decreased c-Myc expression in NPC cells, which were crucial for the decrease in glycolysis and increase in OXPHOS-related protein expression induced by LPLUNC1 over-expression. Finally, we found that treatment with all-trans retinoic acid (ATRA) reduced the viability and clonogenicity of NPC cells, decreased glycolysis and increased OXPHOS-related protein xpression by enhancing LPLUNC1 expression in NPC cells. Therefore, the LPLUNC1-PHB1-p53/c-Myc axis decreased glycolysis in NPC cells and ATRA up-regulated LPLUNC1 expression, a promising drug for intervention of NPC.

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LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1‐p53/c‐Myc axis

Cited by 4 publications

References 64 publications

ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells

ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells

TOM40 regulates the progression of nasopharyngeal carcinoma through ROS-mediated AKT/mTOR and p53 signaling

LPLUNC1 reduces glycolysis in nasopharyngeal carcinoma cells through the PHB1‐p53/c‐Myc axis

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