Expression and function of peroxiredoxins in gynecological malignancies

Zhang, Wenwen; Zhou, Qingfeng; Tao, Xuejiao; Shen, Zefeng; Luo, Hui; Zhu, Xueqiong

doi:10.2741/4435

Cited by 2 publications

(1 citation statement)

References 45 publications

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“…Like Prdx3, the expression of Prdx5 is upregulated in endometrial cancer and this enhanced expression of Prdx5 in the endometrium of females with endometrial tumor can serve as a prognostic marker [167]. Mitochondrial Prdxs are overexpressed in ovarian cancer cells, and Prdx5 serves as a negative predictor of survival in patients suffering from ovarian cancer [180,181,182]. The upregulated expression of Prdx5 is also observed in malignant mesothelioma cells [169], while a reduction in Prdx5 expression has only been described in adrenocortical carcinoma [183].…”

Section: Prdx5 and Carcinogenesismentioning

confidence: 99%

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

Ismail

Kim

Lee

et al. 2019

IJMS

102

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Mitochondria are multifunctional cellular organelles that are major producers of reactive oxygen species (ROS) in eukaryotes; to maintain the redox balance, they are supplemented with different ROS scavengers, including mitochondrial peroxiredoxins (Prdxs). Mitochondrial Prdxs have physiological and pathological significance and are associated with the initiation and progression of various cancer types. In this review, we have focused on signaling involving ROS and mitochondrial Prdxs that is associated with cancer development and progression. An upregulated expression of Prdx3 and Prdx5 has been reported in different cancer types, such as breast, ovarian, endometrial, and lung cancers, as well as in Hodgkin’s lymphoma and hepatocellular carcinoma. The expression of Prdx3 and Prdx5 in different types of malignancies involves their association with different factors, such as transcription factors, micro RNAs, tumor suppressors, response elements, and oncogenic genes. The microenvironment of mitochondrial Prdxs plays an important role in cancer development, as cancerous cells are equipped with a high level of antioxidants to overcome excessive ROS production. However, an increased production of Prdx3 and Prdx5 is associated with the development of chemoresistance in certain types of cancers and it leads to further complications in cancer treatment. Understanding the interplay between mitochondrial Prdxs and ROS in carcinogenesis can be useful in the development of anticancer drugs with better proficiency and decreased resistance. However, more targeted studies are required for exploring the tumor microenvironment in association with mitochondrial Prdxs to improve the existing cancer therapies and drug development.

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Section: Prdx5 and Carcinogenesismentioning

confidence: 99%

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

Ismail

Kim

Lee

et al. 2019

IJMS

102

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Up-regulation of peroxiredoxin-1 promotes cell proliferation and metastasis and inhibits apoptosis in cervical cancer

Lu¹,

Hu²,

Pan³

et al. 2020

J. Cancer

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Objective: To investigate the effect of peroxiredoxin 1 (PRDX1) on the biological behavior of cervical cancer cells and the possible mechanism. Materials and methods: The expression of PRDX1 in human cervical cancer tissues and adjacent non-tumor tissues were detected by immunohistochemistry (IHC). Lentivirus containing PRDX1-cDNA or shRNA against PRDX1 was constructed to overexpress or knockdown PRDX1 in SiHa cervical cancer cells. Cell proliferation was tested by CCK-8 and BrdU incorporation assay and cell apoptosis was evaluated by AnnexinV-PE /7AAD assay. Scratch wound and transwell invasion assay were used to test migration and invasion activity after PRDX1 was overexpressed or suppressed. Furthermore, the effect of PRDX1 on cell proliferation and apoptosis was also studied using a xenograft model of nude mice. Results: The expression of PRDX1 protein was significantly up-regulated in the tumor tissues compared with the paired adjacent non-tumor tissues. Meanwhile, PRDX1 overexpression was associated with tumor stage, lymphatic metastasis and differentiation. Overexpression of PRDX1 significantly promoted proliferation and inhibited apoptosis by increasing the expression of Nanog, proliferating cell nuclear antigen (PCNA), B-cell lymphoma-2 (Bcl-2) and downregulating the expression of Bcl2-associated X protein (BAX) in SiHa cervical cancer cells. Moreover, PRDX1 overexpression increased invasion and migration of SiHa cervical cancer cells via up-regulating the expression of Snail and matrix metalloprotein 9 (MMP-9) and down-regulating the expression of E-cadherin. Knockdown of PRDX1 resulted in the opposite results. The role of PRDX1 in promoting SiHa cervical cancer cell proliferation and inhibiting apoptosis has also been confirmed in vivo in a mouse xenograft model. Conclusions: PRDX1 promoted cell proliferation, migration, and invasion and suppressed apoptosis of cervical cancer possibly via regulating the expression of related protein.

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Expression and function of peroxiredoxins in gynecological malignancies

Cited by 2 publications

References 45 publications

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

Up-regulation of peroxiredoxin-1 promotes cell proliferation and metastasis and inhibits apoptosis in cervical cancer

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