Cytoplasmic localization of Nrf2 promotes colorectal cancer with more aggressive tumors via upregulation of PSMD4

Lin, Pei-Ying; Chang, Jinghua Tsai; Wu, De Wei; Huang, Chun‐Chia; Lee, Huei

doi:10.1016/j.freeradbiomed.2016.03.014

Cited by 33 publications

(36 citation statements)

References 49 publications

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“…For instance, in breast cancer, PSMD4 is shown to be increased and upregulation of PSMD4 is correlated with poor survival . In colorectal cancer, PSMD4 is suggested to be a potential target for inhibiting tumor aggressiveness . In hepatocellular carcinoma (HCC), the expression of PSMD4 was increased and is likely to be associated with dedifferentiation of HCC .…”

Section: Introductionmentioning

confidence: 98%

“…PSMD4 not only plays a role in the regulation of ubiquitin protein degradation, but also participates in the development of biological processes . Abnormal expression of PSMD4 has been widely identified in different cancers . For instance, in breast cancer, PSMD4 is shown to be increased and upregulation of PSMD4 is correlated with poor survival .…”

Section: Introductionmentioning

confidence: 99%

“…17 Proteasome 26S subunit non-ATPase 4 (PSMD4) contains a ubiquitin motif, which interacts with ubiquitination proteins to mediate protein degradation. 18 Related studies have found that deletion of the PSMD4 gene does not affect the survival of yeast, while in other organisms, development is affected by deletion of the PSMD4 gene. 19,20 For instance, PSMD4 knockout in mice is an embryonic lethal mutation.…”

Section: Introductionmentioning

confidence: 99%

“…20 Abnormal expression of PSMD4 has been widely identified in different cancers. 18,21,22 For instance, in breast cancer, PSMD4 is shown to be increased and upregulation of PSMD4 is correlated with poor survival. 21 In colorectal cancer, PSMD4 is suggested to be a potential target for inhibiting tumor aggressiveness.…”

Section: Introductionmentioning

confidence: 99%

“…21 In colorectal cancer, PSMD4 is suggested to be a potential target for inhibiting tumor aggressiveness. 18 In hepatocellular carcinoma (HCC), the expression of PSMD4 was increased and is likely to be associated with dedifferentiation of HCC. 22 These data suggested the oncogenic role of PSMD4 in the progression of tumors.…”

Section: Introductionmentioning

confidence: 99%

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

Zhao

et al. 2019

The Kaohsiung J of Med Scie

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Proteasome 26S subunit non‐ATPase 4 (PSMD4) is an important proteasome ubiquitin receptor and plays a key role in endoplasmic reticulum stress (ERS). However, the study of PSMD4 in esophageal cancer (EC) is relatively rare. Here, we found that the expression of PSMD4 was markedly enhanced in EC tissues and cell lines. The cell counting kit‐8 (CCK‐8) assay showed that overexpression of PSMD4 significantly enhanced Eca109 cell viability, while inhibition of PSMD4 reduced Eca109 cell viability. Knockdown of PSMD4 induced Eca109 cell apoptosis and cell cycle arrest. More importantly, knockdown of PSMD4 significantly enhanced the expression of glucose regulated protein 78, activating transcription factor 6, and p‐protein kinase R‐like ER kinase, indicating an enhanced ERS response in esophageal cancer cells. Compared with the control cells, brefeldin A significantly inhibited the expression of PSMD4 and increased the expression of p53‐upregulated modulator of apoptosis. However, such effects were largely reversed after overexpressing PSMD4 in Eca109 cells, suggesting that silencing PSMD4 could enhance ERS‐induced cell apoptosis. In summary, upregulation of PSMD4 promoted the progression of esophageal cancer mainly by reducing ERS‐induced cell apoptosis.

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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

Zhao

et al. 2019

The Kaohsiung J of Med Scie

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An integrative analysis reveals the prognostic value and potential functions of PSMD11 in hepatocellular carcinoma

Zhang

et al. 2023

Molecular Carcinogenesis

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The global burden of hepatocellular carcinoma (HCC) as a preeminent etiology of cancer‐related mortalities sheds light on the imperative necessity for a more profound comprehension of its fundamental biological mechanisms. In this context, the precise function of the 26S proteasome non‐ATPase regulatory subunit 11 (PSMD11) in HCC remains equivocal. To address this vital knowledge gap, we interrogated the cancer genome atlas, genotype‐tissue expression, International cancer genome consortium, gene expression omnibus, the cancer cell line encyclopedia, and tumor immune single‐cell hub databases to evaluate the expression pattern of PSMD11, further confirmed by reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) in LO2, MHCC‐97H, HepG2, and SMMC7721 cell lines. Additionally, we meticulously assessed the clinical significance and prognostic value of PSMD11, while also exploring its potential molecular mechanisms in HCC. Our findings demonstrated that PSMD11 was highly expressed in HCC tissues, correlating with pathologic stage and histologic grade, thereby conferring a poor prognosis. Mechanistically, PSMD11 appears to exert its tumorigenic effects through the modulation of tumor metabolism‐related pathways. Impressively, low PSMD11 expression was associated with increased immune effector cell infiltration, heightened responsiveness to molecular targeted drugs such as dasatinib, erlotinib, gefitinib, and imatinib, as well as reduced somatic mutation rate. Additionally, we demonstrated that PSMD11 might modulate HCC development through intricate interactions with cuproptosis‐related genes ATP7A, DLAT, and PDHA1. Our comprehensive analyses collectively suggest that PSMD11 represents a promising therapeutic target in HCC.

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Thiadiazole derivatives as anticancer agents

Szeliga

2020

Pharmacol. Rep

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In spite of substantial progress made toward understanding cancer pathogenesis, this disease remains one of the leading causes of mortality. Thus, there is an urgent need to develop novel, more effective anticancer therapeutics. Thiadiazole ring is a versatile scaffold widely studied in medicinal chemistry. Mesoionic character of this ring allows thiadiazole-containing compounds to cross cellular membrane and interact strongly with biological targets. Consequently, these compounds exert a broad spectrum of biological activities. This review presents the current state of knowledge on thiadiazole derivatives that demonstrate in vitro and/or in vivo efficacy across the cancer models with an emphasis on targets of action. The influence of the substituent on the compounds’ activity is depicted. Furthermore, the results from clinical trials assessing thiadiazole-containing drugs in cancer patients are summarized.

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Cytoplasmic localization of Nrf2 promotes colorectal cancer with more aggressive tumors via upregulation of PSMD4

Cited by 33 publications

References 49 publications

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

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

An integrative analysis reveals the prognostic value and potential functions of PSMD11 in hepatocellular carcinoma

Thiadiazole derivatives as anticancer agents

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