TRIM11 suppresses ferritinophagy and gemcitabine sensitivity through UBE2N/TAX1BP1 signaling in pancreatic ductal adenocarcinoma

Shang, Ming; Weng, Li; Xu, Guifang; Wu, Shaoqiu; Liu, Bingyan; Yin, Xiaoxing; Mao, Aiwu; Zou, Xiaoping; Wang, Zhongmin

doi:10.1002/jcp.30346

Cited by 26 publications

(16 citation statements)

References 47 publications

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“…Additionally, TRIM11 can activate MAPK or PI3K/AKT signaling pathways to promote tumor cell proliferation, invasion, and migration 22 . Shang et al identified that TRIM11 suppresses ferritinophagy in pancreatic ductal adenocarcinoma 23 . So, this study elucidates the role and potential mechanism of TRIM11 in ferroptosis of NSCLC.…”

Section: Introductionmentioning

confidence: 77%

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

Liang,

Li,

Zhang

et al. 2023

Clinical Respiratory J

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Lung cancer is one of the leading causes of cancer‐related deaths worldwide, with non‐small cell lung cancer (NSCLC) being the most prevalent type. This study investigates the role of TRIM11 gene in NSCLC and its underlying mechanism. NSCLC patients were recruited from our hospital and showed upregulated TRIM11 mRNA and protein expressions. Patients with high TRIM11 expression had lower survival rates. TRIM11 gene was found to promote cell proliferation and reduce ROS‐induced ferroptosis in NSCLC. Additionally, TRIM11 gene induced AMPK expression and its regulation affected TRIM11's effects on cell proliferation and ferroptosis in NSCLC. IP analysis revealed that TRIM11 protein interacted with AMPK protein in NSCLC. These data confirmed that TRIM11 promotes cell proliferation and reduces ROS‐induced ferroptosis in NSCLC through AMPK. Hence, TRIM11 is a potential target for the treatment of NSCLC and other cancers.

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Section: Introductionmentioning

confidence: 77%

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

Liang,

Li,

Zhang

et al. 2023

Clinical Respiratory J

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“…In this study, we first identified that TRIM11 served as a novel Axin1-binding protein and expanded the role of TRIM11 in GC. Previously, TRIM11 upregulation had been detected in a series of human cancers, such as pancreatic ductal adenocarcinoma, renal clear cell carcinoma, ovarian cancer, and breast cancer [11,20,35]. Luo and Wang showed that TRIM11 upregulation was positively correlated with advanced pathological stage, large tumor size, and poor prognosis in GC [19].…”

Section: Discussionmentioning

confidence: 99%

“…Tripartite motif 11 (TRIM11), a RING-type E3 ubiquitin-protein ligase, is reported to be involved in several human malignant processes, including exacerbated proliferation, metastasis, angiogenesis, and chemoresistance [11][12][13]. Previous studies have shown that TRIM11 is upregulated and associated with tumor growth and metastasis in glioma, lung cancer, hepatocellular cancer, and breast cancer [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

The E3 Ubiquitin Ligase TRIM11 Facilitates Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway via Destabilizing Axin1 Protein

Zhou

Wang

Zhong

et al. 2022

Journal of Oncology

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Background. Aberrant expression of tripartite motif 11 (TRIM11) and the Wnt/β-catenin pathway are essential for facilitating tumorigenesis and progression in multiple types of cancer. Aim. To investigate the molecular changes linking the dysregulation of TRIM11 and Wnt/β-catenin pathway activation in gastric cancer (GC) progression. Methods. The expression levels of TRIM11 were detected in GC tissues and cells by immunohistochemistry and western blotting. The role of TRIM11 in the growth, proliferation, and invasion of gastric cancer cells was observed by a series of cell functional experiments and further verified in vivo. Co-immunoprecipitation (Co-IP), immunofluorescence, cycloheximide, and western blotting assays and other experiments were conducted to explore the mechanisms of TRIM11 underlying the regulation of the Wnt/β-catenin pathway. For further verification, rescue experiments were performed by cotransfection of TRIM11 and Axin1 siRNA in GC cells. Results. Using Co-IP assays, we identified TRIM11 as a potent binding partner of Axin1 in GC cells. Elevated TRIM11 levels were significantly correlated with unfavorable clinical outcomes and poor survival in patients with GC. In addition, TRIM11 promoted the cell proliferation and invasion capacities of GC cells in vitro and tumor growth in vivo. Mechanistic investigations revealed that TRIM11 destabilized Axin1 protein by interacting with Axin1, thus inducing the activation of the Wnt/β-catenin pathway. Moreover, we found that the oncogenic effects of TRIM11 on GC cells were partly mediated by suppression of Axin1. Furthermore, the protein expression of TRIM11 and Axin1 was negatively correlated in GC tissues. Conclusion. Collectively, our findings not only establish a pivotal TRIM11-Axin1-β-catenin axis in driving GC progression but also indicate that TRIM11 serves as a valuable therapeutic target for the treatment of GC patients.

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“…Of note, UBE2N has a similar role to TRIM11 in regulating the autophagic pathway. It was demonstrated that UBE2N interacts with TRIM11, thereby promoting TRIM11-mediated ferritin phagocytosis and resistance to gemcitabine in PC ( 45 ).…”

Section: Class I E2s In Digestive System Cancersmentioning

confidence: 99%

Ubiquitin‑conjugating enzymes as potential biomarkers and therapeutic targets for digestive system cancers (Review)

Lei

et al. 2023

Oncol Rep

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Digestive system cancers are the leading cause of cancer-related death worldwide due to their high morbidity and mortality rates. The current treatment methods include surgical treatment, chemotherapy, radiotherapy and endoscopic treatment, and the precisely targeted therapy of digestive system cancers requires to be further studied. The ubiquitin-proteasome system is the main pathway for protein degradation in cells and the ubiquitin-conjugating enzymes (E2s) have a decisive role in the specific selection of target proteins for degradation. The E2s have an important physiological role in digestive system cancers, which is related to the clinical tumor stage, differentiation degree and poor prognosis. Furthermore, they are involved in the physiological processes of digestive system tumor cell proliferation, migration, invasion, stemness, drug resistance and autophagy. In the present article, the progress and achievements of the E2s in gastric cancer, hepatocellular carcinoma, pancreatic cancer, colorectal cancer, intrahepatic cholangiocarcinoma, gallbladder cancer and esophageal squamous cell carcinoma were reviewed, which may provide early screening indicators and reliable therapeutic targets for digestive system cancers.

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TRIM11 suppresses ferritinophagy and gemcitabine sensitivity through UBE2N/TAX1BP1 signaling in pancreatic ductal adenocarcinoma

Cited by 26 publications

References 47 publications

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

The E3 Ubiquitin Ligase TRIM11 Facilitates Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway via Destabilizing Axin1 Protein

Ubiquitin‑conjugating enzymes as potential biomarkers and therapeutic targets for digestive system cancers (Review)

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