Annexin A5 suppresses cyclooxygenase-2 expression by downregulating the protein kinase C-ζ-nuclear factor-κB signaling pathway in prostate cancer cells

Baek, Hyoung‐Seok; Park, Nahee; Kwon, Yeo‐Jung; Ye, Dong-Jin; Shin, Sungho; Chun, Young‐Jin

doi:10.18632/oncotarget.19392

Cited by 22 publications

(18 citation statements)

References 46 publications

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“…Contrarily, large amounts of research demonstrated ANXA5 acts as tumor suppressor. For instance, ANXA5 can suppress cell proliferation and metastasis in uterine cervical carcinoma ( 13 ); it transfers to the mitochondria, suppressing the voltage-dependent anion channel (VDAC) oligomerization which leads to prostate cancer cell apoptosis ( 14 ). ANXA5 suppresses murine neuroblastoma cell proliferation by blotting PS which results in the enhanced T cell-dependent tumor immunity ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer Cells via ERK Pathway

et al. 2021

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Gastric cancer is one of the most fatal diseases around the world. However, the mechanism of the development of gastric cancer is still not clarified. In addition, the anticancer drugs have cytotoxicity with different degrees. AnnexinA5, a member of the annexin family, has a great binding ability with the membrane phospholipid in a calcium dependent manner and is involved in the development of various cancers. This study aims to explore the influence of annexinA5 on human gastric cancer cells and whether it has the potential to be an auxiliary treatment to gastric cancer. In this study, the role of annexinA5 was detected from both the endogenous and the exogenous aspects on the gastric cancer cell lines MGC-803 and MKN-45. The cells were divided into a knockdown group in which RNA interference technique was used to suppress annexinA5 expression and a protein-supplementing group in which annexinA5 protein was added in the culture supernatant. After the suppression ratio of RNA interference was determined and the IC50 of annexinA5 protein was decided respectively, the cells’ proliferation was detected by MTT assay, colony formation assay, and the expression of PCNA. FCM assay and PI staining methods were applied to test cell apoptosis and necrosis. To investigate whether ANXA5 influence cell metastasis, wound healing assay and transwell assay were employed. To further detect the mechanism of annexinA5 action, the signal pathway was examined with Western Blot method. When ANXA5 gene was knocked down, cell proliferation and metastasis were promoted, while cell apoptosis was suppressed. On the other hand, after the annexinA5 protein was applied to the gastric cancer cells, cell proliferation and metastasis were inhibited, while cell apoptosis and necrosis were promoted. AnnexinA5 played its role via ERK signal pathway. ANXA5 acted as tumor suppressor gene in the gastric cancer by suppressing ERK signal pathway and has the potentiality to be an auxiliary anticancer agent.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer Cells via ERK Pathway

et al. 2021

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“…Knock-out of the prostate apoptosis response 4 ( Par4 ), a pro-apoptotic tumor suppressor gene, results in spontaneous development of prostate cancer in mice, possibly due to loss of negative regulation of the atypical PKCζ and elevated expression of the anti-apoptotic protein XIAP [ 122 ]. Also, inhibition of PKCζ expression by Annexin A5 seems important in repressing COX-2 expression in prostate cancer cells [ 123 ]. This is in line with several observations showing that elevated expression and alternative splicing of PKCζ promotes an aggressive prostate cancer phenotype [ 124 , 125 ].…”

Section: Nf-κb Signaling Pathways In Prostate Cancersmentioning

confidence: 99%

Inflammation and NF-κB Signaling in Prostate Cancer: Mechanisms and Clinical Implications

Staal

Beyaert

2018

Cells

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Prostate cancer is a highly prevalent form of cancer that is usually slow-developing and benign. Due to its high prevalence, it is, however, still the second most common cause of death by cancer in men in the West. The higher prevalence of prostate cancer in the West might be due to elevated inflammation from metabolic syndrome or associated comorbidities. NF-κB activation and many other signals associated with inflammation are known to contribute to prostate cancer malignancy. Inflammatory signals have also been associated with the development of castration resistance and resistance against other androgen depletion strategies, which is a major therapeutic challenge. Here, we review the role of inflammation and its link with androgen signaling in prostate cancer. We further describe the role of NF-κB in prostate cancer cell survival and proliferation, major NF-κB signaling pathways in prostate cancer, and the crosstalk between NF-κB and androgen receptor signaling. Several NF-κB-induced risk factors in prostate cancer and their potential for therapeutic targeting in the clinic are described. A better understanding of the inflammatory mechanisms that control the development of prostate cancer and resistance to androgen-deprivation therapy will eventually lead to novel treatment options for patients.

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“…The effect of PKC on the cell cycle is highly context-dependent and varies depending on the specific isoenzyme involved and other factors, such as the time and duration of enzyme activation [ 122 ]. Some studies suggested that PKC-α, PKC-ε [ 124 ], and the atypical PKCs (aPKCs), PKC-λ/ι [ 125 ] and PKC- ζ [ 124 , 126 ], preferably induce cell proliferation and survival, while PKC-δ regulates apoptosis [ 127 ].…”

Section: Pks and Pc Progressionmentioning

confidence: 99%

Targeting Protein Kinases and Epigenetic Control as Combinatorial Therapy Options for Advanced Prostate Cancer Treatment

et al. 2022

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Prostate cancer (PC), the fifth leading cause of cancer-related mortality worldwide, is known as metastatic bone cancer when it spreads to the bone. Although there is still no effective treatment for advanced/metastatic PC, awareness of the molecular events that contribute to PC progression has opened up opportunities and raised hopes for the development of new treatment strategies. Androgen deprivation and androgen-receptor-targeting therapies are two gold standard treatments for metastatic PC. However, acquired resistance to these treatments is a crucial challenge. Due to the role of protein kinases (PKs) in the growth, proliferation, and metastases of prostatic tumors, combinatorial therapy by PK inhibitors may help pave the way for metastatic PC treatment. Additionally, PC is known to have epigenetic involvement. Thus, understanding epigenetic pathways can help adopt another combinatorial treatment strategy. In this study, we reviewed the PKs that promote PC to advanced stages. We also summarized some PK inhibitors that may be used to treat advanced PC and we discussed the importance of epigenetic control in this cancer. We hope the information presented in this article will contribute to finding an effective treatment for the management of advanced PC.

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Annexin A5 suppresses cyclooxygenase-2 expression by downregulating the protein kinase C-ζ-nuclear factor-κB signaling pathway in prostate cancer cells

Cited by 22 publications

References 46 publications

RETRACTED: AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer Cells via ERK Pathway

RETRACTED: AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer Cells via ERK Pathway

Inflammation and NF-κB Signaling in Prostate Cancer: Mechanisms and Clinical Implications

Targeting Protein Kinases and Epigenetic Control as Combinatorial Therapy Options for Advanced Prostate Cancer Treatment

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