The role of Toll-like receptor 4 signaling pathway in ovarian, cervical, and endometrial cancers

Lupi, Luiz Antônio; Cucielo, Maira Smaniotto; Silveira, Henrique Spaulonci; Gaiotte, Letícia Barbosa; Cesário, Roberta Carvalho; Seiva, Fábio Rodrigues Ferreira; Chuffa, Luiz Gustavo de Almeida

doi:10.1016/j.lfs.2020.117435

Cited by 34 publications

(27 citation statements)

References 82 publications

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“…Consistent with our outcomes, KIAA0101 has been found to be a potential oncogene in multiple cancers such as hepatocellular cancer ( 13), ovarian cancer (14), and breast cancer (20). The toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MYD88) signaling pathway has been found to be implicated in the tumorigenesis and progression of multiple cancers, including CLL (21,22). For instance, MYD88 knockdown inhibited cell proliferation, migration, and invasion in vitro, and inhibited subcutaneous xenograft tumor growth in vivo in colorectal cancer (23).…”

Section: Discussionsupporting

confidence: 82%

KIAA0101 knockdown inhibits cell proliferation and induces cell cycle arrest and cell apoptosis in chronic lymphocytic leukemia cells

et al. 2021

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Background: Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with intense cytogenetic aberrations. Importantly, our recent report indicated that thyroid hormone receptor interactor 13 (TRIP13) is a potential new therapeutic target in CLL. In this study, we predicted 20 TRIP13-related genes and found that KIAA0101 is a novel gene that regulates cell proliferation and the cell cycle of CLL cells.Methods: CD19 + B cells were isolated from the peripheral blood of 26 CLL patients and 6 healthy donors through magnetic cell sorting. Cell proliferation was assessed by the CCK-8 assay. The mRNA and protein levels of genes were examined through RT-qPCR and western blot assays, respectively. Cell cycle and cell apoptosis were measured through Annexin V-based flow cytometry and the caspase 3/7 activity assay.Potential targets of KIAA0101 were identified through microarray analysis. 20 TRIP13 related genes was predicted by Ingenuity Pathway Analysis (IPA). KIAA0101-regulated functions and molecular pathways were predicted through IPA.Results: KIAA0101 knockdown had the strongest inhibitory effect on CLL cell proliferation among the 20 TRIP13-related genes. KIAA0101 was highly expressed in CD19 + B cells of CLL patients. KIAA0101 knockdown induced cell cycle arrest and cell apoptosis, and inhibited FOXO1, MYD88, and TLR4 expression in CLL cells. Conclusions:Taken together, we demonstrated that KIAA0101 plays a critical role in cell proliferation and the cell cycle of human CLL cells. KIAA0101 knockdown induced cell apoptosis, and reduced FOXO1, MYD88, and TLR4 expression, and may therefore be used as a therapeutic target of CLL.

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Section: Discussionsupporting

confidence: 82%

KIAA0101 knockdown inhibits cell proliferation and induces cell cycle arrest and cell apoptosis in chronic lymphocytic leukemia cells

et al. 2021

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“…Toll-like receptor 4, a well-characterized transmembrane protein, is a crucial sensor involved in inflammation and carcinogenesis (Chen et al, 2008;Yang et al, 2019). The TLR4/myeloid differentiation factor 88 (MyD88) pathway has been recognized as oncogenic signaling in human cancers and is correlated with patients' poor survival (Chen et al, 2008;Lupi et al, 2020). It has been shown that HCC promotion depends on TLR4 and that TLR4 is required to mediate cell proliferation (Dapito et al, 2012;Weber et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Inducible Ubiquitin Specific Peptidase 13 Contributes to Tumor Growth and Metastasis via Enhancing the Toll-Like Receptor 4/Myeloid Differentiation Primary Response Gene 88/Nuclear Factor-κB Pathway in Hepatocellular Carcinoma

Gao

Chen

et al. 2020

Front. Cell Dev. Biol.

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“…TLR-4 is the major receptor for LPS recognition, which recruits adaptor proteins via the MyD88-dependent pathway and MyD88-independent pathway to activate NF-κB and amplify its effects (Figure 1) [68]. Based on the fact that 5-FU promotes the expression of TLR-4 in mice more strongly than TLR-2 and G-bacteria proliferate in large numbers during chemotherapy, the TLR-4/MyD88/NF-κB/MAPK pathway may play a central role in the intestinal injury [54].…”

Section: The Relationship Between Cim and Tlr-4 Signalingmentioning

confidence: 99%

Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways

Wei

Wen

Chen

2021

IJMS

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Chemotherapy-induced intestinal mucositis, a painful debilitating condition affecting up to 40–100% of patients undergoing chemotherapy, can reduce the patients’ quality of life, add health care costs and even postpone cancer treatment. In recent years, the relationships between intestinal microbiota dysbiosis and mucositis have drawn much attention in mucositis research. Chemotherapy can shape intestinal microbiota, which, in turn, can aggravate the mucositis through toll-like receptor (TLR) signaling pathways, leading to an increased expression of inflammatory mediators and elevated epithelial cell apoptosis but decreased epithelial cell differentiation and mucosal regeneration. This review summarizes relevant studies related to the relationships of mucositis with chemotherapy regimens, microbiota, TLRs, inflammatory mediators, and intestinal homeostasis, aiming to explore how gut microbiota affects the pathogenesis of mucositis and provides potential new strategies for mucositis alleviation and treatment and development of new therapies.

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The role of Toll-like receptor 4 signaling pathway in ovarian, cervical, and endometrial cancers

Cited by 34 publications

References 82 publications

KIAA0101 knockdown inhibits cell proliferation and induces cell cycle arrest and cell apoptosis in chronic lymphocytic leukemia cells

KIAA0101 knockdown inhibits cell proliferation and induces cell cycle arrest and cell apoptosis in chronic lymphocytic leukemia cells

Hypoxia-Inducible Ubiquitin Specific Peptidase 13 Contributes to Tumor Growth and Metastasis via Enhancing the Toll-Like Receptor 4/Myeloid Differentiation Primary Response Gene 88/Nuclear Factor-κB Pathway in Hepatocellular Carcinoma

Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways

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