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Surgical Research and New Technique

Surgical Research and New Technique >

2019 , Vol. 8 >Issue 1: 49 - 53

DOI: https://doi.org/10.3969/j.issn.2095-378X.2019.01.014

Review

Research progress on TLR4/MyD88 signaling pathway in paclitaxel-resistant ovarian carcinoma

  • WANG Anfeng ,
  • PAN Chen ,
  • TONG Xiaowen
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  • 1.Department of Obstetrics and Gynecology, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, China;
    2.Department of Obstetrics and Gynecology, Liyang Branch, Jiangsu People’s Hospital, Liyang 213300, China

Received date: 2018-12-25

  Online published: 2019-12-09

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Abstract

Gynecological malignancies are one of the important diseases endangering women's health.Ovarian cancer is the most malignant tumour, ranking first in gynecological malignancy death.About 70%-80% of the patients are diagnosed as stage III-IV at their initial visit.Although the treatment methods are ever improving and updating, 80% of the ovarian cancer patients still have a recurrence within one to two years, and the 5-year total survival rate in patients with stage IV ovarian cancer according to International Federation of Gynecology and Obstetrics (FIGO) staging criteria is less than 5%.Studies have shown that paclitaxel, a first-line treatment for immunogenic ovarian cancer, is only 30% effective.Paclitaxel is one of the main ligands of toll-like receptor 4 (TLR4).TLR4 is expressed in all ovarian tissues, and its staining intensity is significantly increased in malignant tumor cells.MyD88 expression is observed in 77.1% ovarian tissues, but not expressed in normal ovarian epithelial tissues, so the high expression of MyD88 is an independent prognostic factor for tumor-free survival and total survival of ovarian carcinoma patients.In epithelial ovarian carcinoma patients with positive MyD88, the activation of TLR4/MyD88-dependent pathway mediates chemoresistance and tumor progression by inflammatory cytokine stimulation, apoptosis inhibition, and immunosuppression, and even promotes cancer cell growth.

Key words： TLR4/MyD88 signaling pathway; Ovarian cancer; Chemoresistance; Negative regulation; Immunosuppression

Cite this article

WANG Anfeng , PAN Chen , TONG Xiaowen . Research progress on TLR4/MyD88 signaling pathway in paclitaxel-resistant ovarian carcinoma[J]. Surgical Research and New Technique, 2019 , 8(1) : 49 -53 . DOI: 10.3969/j.issn.2095-378X.2019.01.014

References

[1] Siegel RL, Miller KD, Jemal A.Cancer Statistics, 2017[J].CA Cancer J Clin, 2017,67(1):7-30.
[2] Xu JH, Hu SL, Shen GD, et al.Tumor suppressor genes and their underlying interactions in paclitaxel resistance in cancer therapy[J].Cancer Cell Int, 2016,16(1):13.
[3] Li Z, Block MS, Vierkant RA, et al.The inflammatory microenvironment in epithelial ovarian cancer:a role for TLR4 and MyD88 and related proteins[J].Tumour Biol, 2016,37(10):13279-13286.
[4] Koti M, Siu A, Clément I, et al.A distinct pre-existing inflammatory tumour microenvironment is associated with chemotherapy resistance in high-grade serous epithelial ovarian cancer[J].Br J Cancer, 2015,113(12):1746.
[5] Zhu Q, Wu X, Wu Y, et al.Interaction between Treg cells and tumor-associated macrophages in the tumor microenvironment of epithelial ovarian cancer[J].Oncol Rep, 2016,36(6):3472-3478.
[6] Wang AC, Ma YB, Wu FX, et al.TLR4 induces tumor growth and inhibits paclitaxel activity in MyD88-positive human ovarian carcinoma in vitro[J].Oncol Lett, 2014,7(3):871-877.
[7] Hemmi H, Takeuchi O, Kawai T, et al.A Toll-like receptor recognizes bacterial DNA[J].Nature, 2000,408(6813):740-745.
[8] Byrd-Leifer C, Block E, Takeda K, et al.The role of MyD88 and TLR4 in the LPS-mimetic activity of Taxol[J].Eur J Immunol, 2001,31(8):2448-2457.
[9] Wu X, Mi Y, Yang H, et al.The activation of HMGB1 as a progression factor on inflammation response in normal human bronchial epithelial cells through RAGE/JNK/NF-kappaB pathway[J].Mol Cell Biochem, 2013,380(1-2):249-257.
[10] Lin JY, Hu GB, Yu CH, et al.Molecular cloning and expression studies of the adapter molecule myeloid differentiation factor 88(MyD88) in turbot (Scophthalmus maximus)[J].Dev & Comp Immunol, 2015,52(2):166-171.
[11] 朱熠,黄建鸣,张国楠,等.卵巢上皮性癌组织中TLR4/MyD88信号通路的表达及其与临床预后的关系[J].中华妇产科杂志, 2013,48(9):694-697.
[12] 李淑青,陈亚萍.卵巢癌对顺铂和紫杉醇耐药的分子机制[J].国际妇产科学杂志, 2016,43(2):145-150.
[13] Wang AC, Su QB, Wu FX, et al.Role of TLR4 for paclitaxel chemotherapy in human epithelial ovarian cancer cells[J].Eur J Clin Invest, 2010,39(2):157-164.
[14] Candido J, Hagemann T.Cancer-related inflammation[J].J Clin Immunol, 2013,33(1):S79-S84.
[15] Wang J Q, Jeelall Y S, Ferguson L L, et al.Toll-like receptors and cancer:MYD88 mutation and inflammation.[J].Front Immunol, 2014,5(367):367.
[16] Xie X, Yang M, Ding Y, et al.Microbial infection, inflammation and epithelial ovarian cancer[J].Oncol Lett, 2017,14(2):1911-1919.
[17] Tadie JM, Bae HB, Jiang S, et al.HMGB1 promotes neutrophil extracellular trap formation through interactions with Toll-like receptor 4[J].Am J Physiol Lung Cell Mol Physiol, 2013,304(5):L342-L349.
[18] Lin Y, Cui M, Xu T, et al.Silencing of cyclooxygenase-2 inhibits the growth,invasion and migration of ovarian cancer cells[J].Mol Med Rep, 2014,9(6):2499.
[19] Ali-Fehmi R, Morris RT, Bandyopadhyay S, et al.Expression of cyclooxygenase-2 in advancedstage ovarian serous carcinoma: correlation with tumor cell proliferation, apoptosis, angiogenesis, and survival[J].Am J Obstet Gynecol, 2005,192(3):819-825.
[20] Athanassiadou P, Grapsa D, Athanassiades P, et al.The prognostic significance of COX-2 and survivin expression in ovarian cancer[J].Pathol Res Pract, 2008,204(4):241-249.
[21] Plewka D, Jakubiecbartnik B, Micha Morek, et al.Survivin in ovary tumors[J].Ginekol Pol, 2015,86(7):525-530.
[22] Li S, Yang Y, Ding Y, et al.Impacts of survivin and caspase-3 on apoptosis and angiogenesis in oral cancer[J].Oncol Lett, 2017,14(3):3774-3779.
[23] Florent M, Anna K, Clement F, et al.Hypoxia induces VEGF-C expression in metastatic tumor cells via a HIF-1α-independent translation-mediated mechanism[J].Cell Rep, 2014,6(1):155.
[24] Miyamoto M, Takano M, Iwaya K, et al.X-chromosome-linked inhibitor of apoptosis as a key factor for chemoresistance in clear cell carcinoma of the ovary[J].Br J Cancer, 2014,110(12):2881-2886.
[25] Chen W, Zeng W, Li X, et al.MicroRNA-509-3p increases the sensitivity of epithelial ovarian cancer cells to cisplatin-induced apoptosis[J].Pharmacogenomics, 2016,17(3):187-197.
[26] Zhang N, Qiu J, Zheng T, et al.Goserelin promotes the apoptosis of epithelial ovarian cancer cells by upregulating forkhead box O1 through the PI3K/AKT signaling pathway[J].Oncol Rep, 2018,39(3):1034-1042.
[27] 邹冬玲,邹冬玲,王冬,等.髓样分化因子促进卵巢癌细胞耐药性的机制研究[J].第三军医大学学报, 2013,35(19):2041-2045.
[28] 王丹,陈晓,徐葳,等.自分泌IL-6经Ras/MEK/ERK、PI3K/Akt通路促进卵巢癌细胞黏附和侵袭功能的研究[J].免疫学杂志, 2016,32(04):294-298.
[29] Duan S, Ying T, Keng P, et al.IL-6 signaling contributes to cisplatin resistance in non-small cell lung cancer via the up-regulation of anti-apoptotic and DNA repair associated molecules[J].Oncotarget, 2015,6(29):27651-27660.
[30] Schwab C L, English D P, Roque D M, et al.Past,present and future targets for immunotherapy in ovarian cancer[J].Immunotherapy, 2014,6(12):1279-1293.
[31] Ying X, Li-Ya Q, Feng Z, et al.MiR-939 promotes the proliferation of human ovarian cancer cells by repressing APC2 expression[J].Biomed Pharmacother, 2015,71(4):64-69.
[32] Bridget C, Kirsten B M, Kimberly R K, et al.Large-scale evaluation of common variation in regulatory T cell-related genes and ovarian cancer outcome[J].Cancer Immunol Res, 2014,2(4):332-340.
[33] 张国楠,朱熠,黄建鸣.对靶向MyD88、IDO1和AHR为中心的免疫抑制信号通路和卵巢上皮性癌免疫治疗的思考[J].中华妇产科杂志, 2018.53(7):448-451.
[34] Whynott R M, Manahan P, Geisler J P.Vascular endothelial growth factor(VEGF) and cyclooxygenase 2(COX 2) immunostaining in ovarian cancer[J].Eur J Gynaecol Oncol, 2016,37(2):164-166.
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