NOD2 inhibits the proliferation of esophageal adenocarcinoma cells through autophagy

Li, Xiaozhi; Liu, Suo; Jin, Longyu; Ma, Yuchao; Liu, Tao

doi:10.1007/s00432-022-04354-x

Cited by 3 publications

(3 citation statements)

References 40 publications

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“…However, its involvement in tumors is diverse and remains incompletely elucidated. Previous research has revealed that NOD2 functions as an immunosurveillance factor in certain types of cancers, such as colorectal 14 and esophageal adenocarcinomas 13 , where it is considered protective. Conversely, aberrant activation of NOD2 has been implicated in liver 16 and cervical 15 cancers, leading to excessive in ammation that promotes tumor development.…”

Section: Discussionmentioning

confidence: 99%

“…Recent investigations have pointed out that aberrant NOD2 expression is tied to cancer progression. NOD2 was reported to inhibit the proliferation of esophageal adenocarcinoma cells via autophagy 13 , whereas its de ciency promoted colorectal tumorigenesis 14 . In addition, the upregulation of NOD2 enhanced the proliferation, invasion, and migration of cervical squamous cell carcinoma 15 .…”

Section: Introductionmentioning

confidence: 99%

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NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

Zhu,

Yun,

et al. 2024

Preprint

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Nucleotide-binding oligomerization domain 2 (NOD2) is an immune sensor crucial for eliciting the innate immune responses. Nevertheless, discrepancies exist regarding the effect of NOD2 on different types of cancer. The aim of this study was to investigate the function of NOD2 in melanoma and its underlying mechanisms. We have validated the tumor suppressor effect of NOD2 in melanoma. NOD2 inhibited the proliferation of melanoma cells, hindering their migration and invasion while promoting the onset of apoptosis. Our study showed that NOD2 expression is closely related to folate metabolism, and its mechanism of action is to inhibit TYMS expression by promoting ubiquitination modification of thymidylate synthase (TYMS), thereby decreasing the resistance of melanoma cells to 5-fluorouracil (5-FU) and capecitabine (CAP). TYMS was identified to form a complex with Polo-like Kinase 1 (PLK1) and activate the PLK1 signaling pathway. Furthermore, we revealed that the combination of the PLK1 inhibitor volasertib (BI6727) with 5-FU or CAP had a synergistic effect repressing the proliferation and migration of melanoma cells. Overall, our research highlights the protective role of NOD2 in melanoma and suggests that targeting NOD2 and the TYMS/PLK1 signaling axis is a high-profile therapy that could be a prospect for melanoma treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

Zhu,

Yun,

et al. 2024

Preprint

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“…Thus, targeting ATG proteins may be useful for efficient EC treatment because it would regulate autophagy 167 . As an innate immune receptor for bacteriogenic components activated by muramyl dipeptide (MDP), nucleotide binding oligomerization domain containing 2 (NOD2) was found to be decreased in EC cells, and further study demonstrated that NOD2 overexpression promoted autophagy in and inhibited the proliferation of EAC cells by acting on the ATG16L1 pathway 168 . In addition, there has been very little research on the usage of ATG modulators in EC.…”

Section: Targeting Autophagy Pathways With Small-molecule Compounds I...mentioning

confidence: 99%

Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics

Zhang¹,

Zhang²,

Luan³

et al. 2023

Int. J. Biol. Sci.

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Esophageal cancer (EC) is the sixth most common and the seventh most deadly malignancy of the digestive tract, representing a major global health challenge. Despite the availability of multimodal therapeutic strategies, the existing EC treatments continue to yield unsatisfactory results due to their limited efficacy and severe side effects. Recently, knowledge of the subroutines and molecular mechanisms of regulated cell death (RCD) has progressed rapidly, enhancing the understanding of key pathways related to the occurrence, progression, and treatment of many types of tumors, including EC. In this context, the use of small-molecule compounds to target such RCD subroutines has emerged as a promising therapeutic strategy for patients with EC. Thus, in this review, we firstly discussed the risk factors and prevention of EC. We then outlined the established treatment regimens for patients with EC. Furthermore, we not only briefly summarized the mechanisms of five best studied subroutines of RCD related to EC, including apoptosis, ferroptosis, pyroptosis, necroptosis and autophagy, but also outlined the recent advances in the development of small-molecule compounds and long non-coding RNA (lncRNA) targeting the abovementioned RCD subroutines, which may serve as a new therapeutic strategy for patients with EC in the future.

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NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

Yun,

Wu,

et al. 2024

Cell Death Dis

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Nucleotide-binding oligomerization domain 2 (NOD2) is an immune sensor crucial for eliciting the innate immune responses. Nevertheless, discrepancies exist regarding the effect of NOD2 on different types of cancer. This study aimed to investigate these function of NOD2 in melanoma and its underlying mechanisms. We have validated the tumor suppressor effect of NOD2 in melanoma. NOD2 inhibited the proliferation of melanoma cells, hindering their migration and invasion while promoting the onset of apoptosis. Our study showed that NOD2 expression is closely related to pyrimidine and folate metabolism. NOD2 inhibits thymidylate synthase (TYMS) expression by promoting K48-type ubiquitination modification of TYMS, thereby decreasing the resistance of melanoma cells to 5-fluorouracil (5-FU) and capecitabine (CAP). TYMS was identified to form a complex with Polo-like Kinase 1 (PLK1) and activate the PLK1 signaling pathway. Furthermore, we revealed that the combination of the PLK1 inhibitor volasertib (BI6727) with 5-FU or CAP had a synergistic effect repressing the proliferation, migration, and autophagy of melanoma cells. Overall, our research highlights the protective role of NOD2 in melanoma and suggests that targeting NOD2 and the TYMS/PLK1 signaling axis is a high-profile therapy that could be a prospect for melanoma treatment.

show abstract

NOD2 inhibits the proliferation of esophageal adenocarcinoma cells through autophagy

Cited by 3 publications

References 40 publications

NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics

NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis

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