Rhomboid domain containing 1 inhibits cell apoptosis by upregulating AP‐1 activity and its downstream target Bcl‐3

Ren, Xiaoxia; Song, Wei; Liu, Wenjie; Guan, Xin; Miao, Fei; Miao, Shiying; Wang, Linfang

doi:10.1016/j.febslet.2013.04.033

Cited by 26 publications

(18 citation statements)

References 38 publications

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“…AP-1 binds 7 different sites in the EGFR promoter, and heterogeneous expression of c-Jun promotes EGFR expression [30]. Our previous work demonstrated that RHBDD1 positively increases c-Jun expression [28]. Taken together, these results establish the RHBDD1-c-Jun-EGFR axis.…”

Section: Discussionmentioning

confidence: 76%

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RHBDD1 upregulates EGFR via the AP-1 pathway in colorectal cancer

et al. 2017

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Our previous study showed that RHBDD1 can activate the EGFR signaling pathway to promote colorectal cancer growth. In the present study, EGFR was decreased when RHBDD1 was knocked down or inactivated. Further analysis found that c-Jun and EGFR protein expression was decreased in RHBDD1 knockdown and inactivated cells. c-Jun overexpression in RHBDD1-inactivated cells rescued EGFR expression in a dose-dependent manner. RHBDD1 overexpression in RHBDD1-inactivated cells restored EGFR expression, but this effect was counteracted by c-Jun knockdown. Furthermore, EGFR and c-Jun were attenuated in the RHBDD1 knockdown and inactivated groups in animal tumor models. Tissue microarray assays demonstrated a correlation between RHBDD1 and EGFR in colorectal cancer patients. Therefore, our findings indicate that RHBDD1 stimulates EGFR expression by promoting the AP-1 pathway.

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Section: Discussionmentioning

confidence: 76%

“…Our previous study showed that RHBDD1 can positively activate c-Jun expression [28]. Other reports have shown that c-Jun increases EGFR mRNA expression [29, 30].…”

Section: Resultsmentioning

confidence: 99%

RHBDD1 upregulates EGFR via the AP-1 pathway in colorectal cancer

et al. 2017

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“…It has been reported that c-Jun -/-fibroblasts are resistant to alkylating agent-induced apoptosis, which may be mediated by Fas ligand induction (17). Additionally, rhomboid domain-containing 1 inhibits UV-induced cell apoptosis by activating and upregulating c-Jun and its downstream target B-cell lymphoma 3 (Bcl-3) (18). c-Fos downregulation in MCF-7/ADR cells resulted in enhanced apoptosis, and altered expression of apoptosis-associated proteins, including Bax, Bcl-2, p53 and PUMA (19).…”

Section: Introductionmentioning

confidence: 99%

Activator protein 1 promotes gemcitabine-induced apoptosis in pancreatic cancer by upregulating its downstream target Bim

Ren

Zhao

et al. 2016

Oncology Letters

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Abstract. Gemcitabine is a commonly used chemotherapy drug in pancreatic cancer. The function of activator protein 1 (AP-1) is cell-specific, and its function depends on the expression of other complex members. In the present study, we added gemcitabine to the media of Panc-1 and SW1990 cells at clinically achieved concentrations (10 µM). Compared with constitutive c-Fos expression, c-Jun expression increased in a dose-dependent manner upon gemcitabine treatment. c-Jun overexpression increased gemcitabine-induced apoptosis through Bim activation, while cell apoptosis and Bim expression decreased following c-Jun knockdown. Furthermore, gemcitabine-induced apoptosis and Bim levels decreased when c-Jun phosphorylation was blocked by SP600125. Our findings suggest that c-Jun, which is a member of the AP-1 complex, functions in gemcitabine-induced apoptosis by regulating its downstream target Bim in pancreatic cancer cells.

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“…The rhomboid family of genes is highly conserved, encoding a group of seven transmembrane proteins which function in diverse processes, including protein cleavage, signaling pathway modulation 92 , 93 , apoptosis 94 , mitochondrial membrane fusion 95 , endoplasmic reticulum-associated degradation 96 , and others. Recent research has highlighted a connection between the RHBDF1 gene and a variety of human diseases, such as leukemia 97 and breast cancer 98 , and research into gene silencing therapies is ongoing 99 .…”

Section: Rna Interference (Rnai)mentioning

confidence: 99%

Nanoparticle-Based Targeted Therapeutics in Head-And-Neck Cancer

Wu¹,

Zhou²

2015

Int. J. Med. Sci.

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Head-and-neck cancer is a major form of the disease worldwide. Treatment consists of surgery, radiation therapy and chemotherapy, but these have not resulted in improved survival rates over the past few decades. Versatile nanoparticles, with selective tumor targeting, are considered to have the potential to improve these poor outcomes. Application of nanoparticle-based targeted therapeutics has extended into many areas, including gene silencing, chemotherapeutic drug delivery, radiosensitization, photothermal therapy, and has shown much promise. In this review, we discuss recent advances in the field of nanoparticle-mediated targeted therapeutics for head-and-neck cancer, with an emphasis on the description of targeting points, including future perspectives.

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Rhomboid domain containing 1 inhibits cell apoptosis by upregulating AP‐1 activity and its downstream target Bcl‐3

Cited by 26 publications

References 38 publications

RHBDD1 upregulates EGFR via the AP-1 pathway in colorectal cancer

RHBDD1 upregulates EGFR via the AP-1 pathway in colorectal cancer

Activator protein 1 promotes gemcitabine-induced apoptosis in pancreatic cancer by upregulating its downstream target Bim

Nanoparticle-Based Targeted Therapeutics in Head-And-Neck Cancer

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