TIPE2 sensitizes osteosarcoma cells to cis-platin by down-regulating MDR1 via the TAK1- NF-κB and - AP-1 pathways

Zhao, Peiqing; Wang, Sujie; Jiang, Jie; Liu, Hong; Zhu, Xiaolan; Zhao, Ning; Li, Jigang; Yin, Yingchun; Pan, Xiaoyan; Yang, Xiaohe; Jian-ping, Guo; Xu, Wenlin

doi:10.1016/j.molimm.2018.08.010

Cited by 23 publications

(18 citation statements)

References 46 publications

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“…The activation of Myd88 recruits two IL-1R-associated kinases (IRAK1 and IRAK4), leading to TNF receptor-associated factor 6 (TRAF6) activation. The activated TRAF6 is ubiquitinated and recruited to the TAK1/TAB protein complex, activating the signaling cascades of AP-1, NF-κB, and MAPKs [36,37,38]. To better elucidate the anti-inflammatory responses of KA at the molecular level, inflammatory responses were induced by MyD88 overexpression.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling

Kim

Shin

Chung

et al. 2019

Cells

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The current treatment options for inflammatory bowel disease (IBD) are unsatisfactory. Therefore, novel and safer therapies are needed. We previously reported that koreanaside A (KA) showed high radical scavenging activity and suppressed vascular cell adhesion molecule 1 (VCAM-1) expression in vascular smooth muscle cells. However, the molecular mechanisms involved in its anti-inflammatory effect have not been reported. KA inhibited pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO), and prostaglandin E2 (PGE2). KA inhibited the production and mRNA expression of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) induced by LPS. KA downregulated the myeloid differentiation primary response 88 (MyD88)-dependent inflammatory gene expressions in the MyD88-overexpressed cells. KA suppressed the LPS-induced transcriptional and DNA-binding activities of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-κB). KA was found to inhibit the phosphorylation of Janus kinase 1/2 (JAK1/2) and signal transducers and activators of transcription 1/3 (STAT1/3). In DSS-induced colitis mice, KA relieved the symptoms of colitis by suppressing inflammatory cell infiltration, restoring tight junction (TJ)- and epithelial–mesenchymal transition (EMT)-related protein expression, and inactivating AP-1, NF-κB, and STAT1/3. Therefore, KA reduced inflammatory responses by downregulating AP-1, NF-κB, and JAK/STAT signaling in LPS-induced macrophages and DSS-induced colitis mice.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling

Kim

Shin

Chung

et al. 2019

Cells

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“…Our group documented that TIPE2 serves as a negative regulator in certain inflammatory diseases (20–22). Moreover, TIPE2 can sensitize osteosarcoma cells to cis-platin by downregulating MDR1 transcription, while TIPE1 promotes cervical cancer progression (16, 23). Thus, based on their implications in the development and progression of a variety of cancers (9, 10, 12, 24), their roles, especially regarding carcinogenesis, need to be fully evaluated.…”

Section: Discussionmentioning

confidence: 99%

TIPE1 Inhibits Breast Cancer Proliferation by Downregulating ERK Phosphorylation and Predicts a Favorable Prognosis

Chen

Liu

et al. 2019

Front. Oncol.

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TIPE1, which acts as a cell death regulator, has emerged as a tumor suppressor in the process of carcinogenesis. However, our recent research demonstrated that it serves as an oncogene in the pathogenesis of cervical cancer, indicating that the role of TIPE1 in carcinogenesis needs to be further evaluated. In this study, we show that TIPE1 is able to inhibit breast cancer cell growth both in vivo and in vitro . Functionally, TIPE1 inhibits cancer cell proliferation preferentially by downregulating ERK phosphorylation. Furthermore, the expression of TIPE1 is decreased in breast cancer tissues compared to matched adjacent tissues, and its expression is positively correlated with patients' lifespan. These data indicate that TIPE1 suppresses breast cancer proliferation by inhibiting the ERK signaling pathway. This study also suggests that TIPE1 could serve as a potential therapeutic target and a diagnostic biomarker for breast cancer.

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“…In detail, the sorafenib-resistant cell line (HepG2/SF) was plated into 96-well plates with a total of 2×10 3 cells/well and subsequently treated with sorafenib (concentrations ranged between 0 and 15 µM) at 37°C for 24 h following transfection with or without PDCD2. The cytotoxicity index was calculated as (1-OD450 of drug-treated cells/OD450 of untreated cells) ×100 according to a previous study (18). The IC50 values of sorafenib were calculated using GraphPad Prism 5 (GraphPad Software, Inc., La Jolla, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

PDCD2 sensitizes HepG2 cells to sorafenib by suppressing epithelial‑mesenchymal transition

Liu

Wang

Liang³

et al. 2019

Mol Med Report

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Epithelial-mesenchymal transition (EMT) has an established role in the acquisition of therapeutic resistance. Programmed cell death domain 2 (PDCD2) is involved in the progression of multiple types of cancer. However, its mechanism underlying chemoresistance in liver cancer has not been elucidated. In the present study, it was demonstrated that the sorafenib-resistant HepG2 cell line exhibited EMT and multidrug resistance (MDR) phenotypes, and reduced expression of PDCD2, by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot analysis and Cell Counting Kit-8. Annexin V/fluorescein isothiocyanate and cell migration assays further demonstrated that PDCD2 effectively promoted sorafenib-induced cell apoptosis and reduced cell metastasis. Mechanistically, PDCD2 inhibited the expression of Vimentin and increased the expression of E-cadherin in a Snail-dependent manner by RT-qPCR and western blot analysis. In conclusion, the present study elucidated for the first time, to the best of our knowledge, that PDCD2 sensitizes sorafenib-resistant HepG2 cells to sorafenib by the downregulation of EMT. PDCD2 may serve as a potential therapeutic target in the treatment of sorafenib-resistant liver cancer.

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TIPE2 sensitizes osteosarcoma cells to cis-platin by down-regulating MDR1 via the TAK1- NF-κB and - AP-1 pathways

Cited by 23 publications

References 46 publications

Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling

Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling

TIPE1 Inhibits Breast Cancer Proliferation by Downregulating ERK Phosphorylation and Predicts a Favorable Prognosis

PDCD2 sensitizes HepG2 cells to sorafenib by suppressing epithelial‑mesenchymal transition

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