NOD1 activation promotes cell apoptosis in papillary thyroid cancer

Bai, Ning; Liu, Chunyan; Zhang, Xiaole; Cheng, Yang; Hou, Deqiang

doi:10.1016/j.prp.2022.153880

Cited by 3 publications

(3 citation statements)

References 34 publications

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“…Furthermore, as compared to normal epithelial cells NTHY-ORI 3-1, NOD1 expression was dramatically enhanced in papillary thyroid cancer (PTC) cell lines such as TPC-1, BCPAP, and KTC-1. NOD1 activation enhanced PTC cell death via caspase-3 and caspase-9 pathways mediated by RIP2/TAK1 and MAPK pathways, whereas NOD1 depletion boosted PTC cell growth in vitro [ 23 ].…”

Section: Nod1 and Nod2 In Cancermentioning

confidence: 99%

“…However, the role of NOD1 and NOD2 in cancer is complicated, indicating that more studies in this field are necessary. It has been found that NOD1 activation contributes to tumor suppression mainly through RIP2/TAK1/ MAPK pathway-mediated apoptosis in oral cancer [45], thyroid cancer [23], breast cancer [26], and GC 27, whereas NOD1 overexpression is associated with tumor development with decreased chemotherapy sensitivity but enhanced immunosuppression in HNSCC 24, ESCC25, prostate cancer [33], and ovarian cancer [36]. Based on those studies, we examined the conflicting roles of NOD1 in HCC [28,29], CRC [22,[30][31][32], and cervical cancer [34,35] and found that NOD1-regulated apoptotic activation is a common feature in tumor suppression, whereas NOD1-mediated immunosuppression is another comparable characteristics in NOD1promoted malignancy which has been described by several studies [31,32].…”

Section: Can Nod1 and Nod2 Be Promising +Erapeutic Targets?mentioning

confidence: 99%

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NOD1 and NOD2 Are Potential Therapeutic Targets for Cancer Immunotherapy

Wang

2022

Computational Intelligence and Neuroscience

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The nucleotide oligomerization domain (NOD)-like receptors (NLRs) are a group of intracellular proteins that are essential for controlling the host's innate immune response. The cytosolic nucleotide binding oligomerization domains 1 and 2 receptors (NOD1 and NOD2) are the most widely investigated NLRs. As pattern recognition receptors (PRRs), NOD1 and NOD2 may recognize and bind endogenous damage associated molecular patterns (DAMPs) and external pathogenic associated molecular patterns (PAMPs), directing the activation of inflammatory caspases through engaging the adaptor protein RIP2, which further activates the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways, thereby mediating host innate immunity and regulating the adaptive immunity. Previous research has identified NOD1 and NOD2 as key players in inflammatory disease and host-microbial defense. Despite numerous studies claiming that NOD1 and NOD2 are linked to tumorigenesis and tumor development, it is still unclear whether NOD1 and NOD2 act as cancer's friends or foes. In this review, we focus on concluding the current research progress on the role of NOD1 and NOD2 in a variety of cancers and discussing the potential reasons for the contradicting role of NOD1 and NOD2 in cancers. This review may help better understand the role of NOD1 and NOD2 in cancer and shed light on NOD1 and NOD2 as potential therapeutic targets for tumor immunotherapy.

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Section: Nod1 and Nod2 In Cancermentioning

confidence: 99%

Section: Can Nod1 and Nod2 Be Promising +Erapeutic Targets?mentioning

confidence: 99%

NOD1 and NOD2 Are Potential Therapeutic Targets for Cancer Immunotherapy

Wang

2022

Computational Intelligence and Neuroscience

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“…Intertumoral activation of NOD1 by the gram-negative bacterial peptidoglycan gTri-DAP can enhance the immunosuppressive activity of myeloid cells to foster a tumor-permissive microenvironment in colon cancer ( Maisonneuve et al, 2021 ). Conversely, NOD1 can induce cell apoptosis and inhibit cell proliferation in papillary thyroid carcinoma and hepatocellular carcinoma ( Bai et al, 2022 ; Ma et al, 2020 ). Most previous studies have focused on NOD1-mediated inflammation and activation of the NF-κB and MAPK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Microbiota enterotoxigenic Bacteroides fragilis-secreted BFT-1 promotes breast cancer cell stemness and chemoresistance through its functional receptor NOD1

Ma,

Zhang,

Chen

et al. 2024

Protein &Amp; Cell

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Tumor-resident microbiota in breast cancer promote cancer initiation and malignant progression. However, targeting microbiota to improve the effects of breast cancer therapy has not been investigated in detail. Here, we evaluated the microbiota composition of breast tumors and found that enterotoxigenic Bacteroides fragilis (ETBF) was highly enriched in the tumors of patients who did not respond to taxane-based neoadjuvant chemotherapy. ETBF, albeit at low biomass, secreted the toxic protein BFT-1 to promote breast cancer cell stemness and chemoresistance. Mechanistic studies showed that BFT-1 directly bound to NOD1 and stabilized NOD1 protein. NOD1 was highly expressed on ALDH+ breast cancer stem cells (BCSCs) and cooperated with GAK to phosphorylate NUMB and promote its lysosomal degradation, thereby activating the NOTCH1-HEY1 signaling pathway to increase BCSCs. NOD1 inhibition and ETBF clearance increases the chemosensitivity of breast cancer by impairing BCSCs.

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