PSMD4 regulates the malignancy of esophageal cancer cells by suppressing endoplasmic reticulum stress

Ma, Aiguo; Yu, Limei; Zhao, Hong; Qin, Cun-Wei; Tian, Xiangyu; Wang, Qing

doi:10.1002/kjm2.12093

Cited by 18 publications

(12 citation statements)

References 35 publications

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“…Recent studies indicate that ERS plays a key role in tumor progression. The initiation of ERS signaling can induce apoptosis in esophageal cancer cells (16,17), which may represent a novel insight for the therapeutic intervention of esophageal cancer. Several studies have demonstrated the role of E2 treatment in enhancing ERS in a few tumors (18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Interaction of Estradiol and Endoplasmic Reticulum Stress in the Development of Esophageal Carcinoma

Wang

Liu

et al. 2020

Front. Endocrinol.

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Gender differences in esophageal cancer patients indicate that estradiol may have antitumor effects on esophageal cancer. The initiation of endoplasmic reticulum stress (ERS) can induce apoptosis in esophageal cancer cells. However, it is still unknown whether estradiol inhibits the development of esophageal cancer by activating ERS pathway. In this study, the gender difference in the development of esophageal cancer was observed by analyzing clinical data and the experimental tumor xenografts in mice. Meanwhile, we investigated the mechanism of ERS in estradiol-mediated inhibition of esophageal cancer using esophageal squamous cell carcinoma cell line EC109. The proportion of male patients with esophageal cancer was significantly higher than female patients. Meanwhile, male patients were prone to have adventitial invasion. The weight of transplanted tumors in female mice was significantly smaller than that in male mice. In vitro experiments showed estradiol inhibits the viability and migration of EC109 cells by increasing the expression of ERS-related proteins, whereas ERS inhibitor 4-PBA abolished the effects of estradiol. In conclusion, our data demonstrate that sex difference exists in the occurrence of esophageal cancer. Estradiol can inhibit the viability and migration of esophageal cancer cells through the activation of ERS, providing a novel insight for esophageal cancer development, treatment, and prevention.

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Section: Introductionmentioning

confidence: 99%

Interaction of Estradiol and Endoplasmic Reticulum Stress in the Development of Esophageal Carcinoma

Wang

Liu

et al. 2020

Front. Endocrinol.

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“…The ER chaperone protein BIP is a major regulatory factor of ER homeostasis and stress response (Li et al, 2016). Many factors can cause ER homeostasis to be disrupted, including bacterial infection (Ma et al, 2019). Studies have found that microbial infection can trigger ERS, and ERS-activating cells can regulate the expression and activation of ERS-related proapoptotic molecules, ultimately determining whether cells are adaptive or undergo apoptosis (Ma et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Many factors can cause ER homeostasis to be disrupted, including bacterial infection (Ma et al, 2019). Studies have found that microbial infection can trigger ERS, and ERS-activating cells can regulate the expression and activation of ERS-related proapoptotic molecules, ultimately determining whether cells are adaptive or undergo apoptosis (Ma et al, 2019). This response allows pro-inflammatory molecules to be released during the chronic inflammation of the CD, leading to damage to the colon cells, and thereby impairing the integrity of the epithelial barrier.…”

Section: Introductionmentioning

confidence: 99%

Fusobacterium nucleatum Activates Endoplasmic Reticulum Stress to Promote Crohn’s Disease Development via the Upregulation of CARD3 Expression

et al. 2020

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There is increasing evidence that members of the gut microbiota, especially Fusobacterium nucleatum (F. nucleatum), are associated with Crohn's disease (CD), but the specific mechanism by which F. nucleatum promotes CD development is unclear. Here, we first examined the abundance of F. nucleatum and its effects on CD disease activity and explored whether F. nucleatum aggravated intestinal inflammation and promoted intestinal mucosal barrier damage in vitro and in vivo. Our data showed that F. nucleatum was enriched in 41.21% of CD tissues from patients and was correlated with the clinical course, clinical activity, and refractory behavior of CD (P < 0.05). In addition, we found that F. nucleatum infection is involved in activating the endoplasmic reticulum stress (ERS) pathway during CD development to promote intestinal mucosal barrier destruction. Mechanistically, F. nucleatum targeted caspase activation and recruitment domain 3 (CARD3) to activate the ERS pathway and promote F. nucleatum-mediated mucosal barrier damage in vivo and in vitro. Thus, F. nucleatum coordinates a molecular network involving CARD3 and ERS to control the CD process. Measuring and targeting F. nucleatum and its associated pathways will provide valuable insight into the prevention and treatment of CD.

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“…They can promote cell proliferation and cell cycle progression prognosis in breast cancer cell lines ( Oguro et al, 2015 ; Okumura et al, 2018 ; Fararjeh et al, 2019 ; Zhao et al, 2020 ). In esophageal cancer, upregulation of PSMD4 can reduce endoplasmic reticulum stress-induced cell apoptosis to promote tumor progression ( Ma et al, 2019 ). It was also reported that PSMD9 was correlated with recurrence after radiotherapy in cervical cancer and can predict radiotherapy benefits in breast cancer ( Langlands et al, 2014 ; Köster et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Prognostic Implication and Immunological Role of PSMD2 in Lung Adenocarcinoma

Zhao

2022

Front. Genet.

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Background: Although previous studies reported that 26S proteasome non-ATPase regulatory subunit 2 (PSMD2) is involved in many human cancers. However, its clinical significance and function in lung adenocarcinoma remain unclear. Here, we examined the prognostic and immunological role of PSMD2 in lung adenocarcinoma.Methods: The Cancer Genome Atlas (TCGA) was conducted to analyze PSMD2 expression and verified using UALCAN. PrognoScan and Kaplan-Meier curves were utilized to assess the effect of PSMD2 on survival. cBioPortal database was conducted to identify the mutation characteristics of PSMD2. Functional enrichment was performed to determine PSMD2-related function. Cancer Single-cell State Atlas (CancerSEA) was used to explore the cancer functional status of PSMD2 at single-cell resolution. PSMD2-related immune infiltration analysis was conducted. Tumor-Immune system interaction database (TISIDB) was performed to verify the correlation between PSMD2 expression and tumor-infiltrating lymphocytes (TILs).Results: Both mRNA and protein expression of PSMD2 were significantly elevated in lung adenocarcinoma. High expression of PSMD2 was significantly correlated with high T stage (p = 0.014), lymph node metastases (p < 0.001), and TNM stage p = 0.005). Kaplan-Meier curves indicated that high expression of PSMD2 was correlated with poor overall survival (38.2 vs. 59.7 months, p < 0.001) and disease-specific survival (59.9 months vs. not available, p = 0.004). Multivariate analysis suggested that PSMD2 was an independent biomarker for poor overall survival (HR 1.471, 95%CI, 1.024–2.114, p = 0.037). PSMD2 had a high mutation frequency of 14% in lung adenocarcinoma. The genetic mutation of PSMD2 was also correlated with poor overall survival, disease-specific survival, and progression-free survival in lung adenocarcinoma. Functional enrichment suggested PSMD2 expression was involved in the cell cycle, RNA transport, and cellular senescence. CancerSEA analysis indicated PSMD2 expression was positively correlated with cell cycle, DNA damage, and DNA repair. Immune infiltration analysis suggested that PSMD2 expression was correlated with immune cell infiltration levels and abundance of TILs.Conclusion: The upregulation of PSMD2 is significantly correlated with poor prognosis and immune infiltration levels in lung adenocarcinoma. Our findings suggest that PSMD2 is a potential biomarker for poor prognosis and immune therapeutic target in lung adenocarcinoma.

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PSMD4 regulates the malignancy of esophageal cancer cells by suppressing endoplasmic reticulum stress

Cited by 18 publications

References 35 publications

Interaction of Estradiol and Endoplasmic Reticulum Stress in the Development of Esophageal Carcinoma

Interaction of Estradiol and Endoplasmic Reticulum Stress in the Development of Esophageal Carcinoma

Fusobacterium nucleatum Activates Endoplasmic Reticulum Stress to Promote Crohn’s Disease Development via the Upregulation of CARD3 Expression

Prognostic Implication and Immunological Role of PSMD2 in Lung Adenocarcinoma

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