A review shows that ATG10 has been identified as a potential prognostic marker and therapeutic target for cancer patients based on real-world studies
- Ke Shi 1, Di Ke 2, Feng Li 2, Rong-Shu Shi 2, Tao Liu 3, Dan Li 4, Qun-Xian Zhang 3
- 1Department of Thoracic Surgery, Beilun District People's Hospital of Ningbo, Ningbo, China.
- 2Department of Radiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
- 3Department of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
- 4Department of Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
- 0Department of Thoracic Surgery, Beilun District People's Hospital of Ningbo, Ningbo, China.
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View abstract on PubMed
Summary
This summary is machine-generated.Autophagy-related gene 10 (ATG10) promotes cancer growth and metastasis. Inhibiting ATG10 may offer a new therapeutic strategy for various cancers, as its overexpression correlates with poor prognosis.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Autophagy-related genes (ATGs) are critical in cancer development and progression.
- ATG10, an ATG family member, is frequently overexpressed in multiple cancers, correlating with poor prognosis and advanced disease.
- ATG10 influences tumorigenesis by affecting epithelial-mesenchymal transition and cell cycle regulation.
Purpose Of The Study
- To review the functional and clinical significance of ATG10 in various cancers.
- To highlight ATG10's potential as a diagnostic biomarker and therapeutic target.
Main Methods
- Literature review of studies on ATG10 in cancer.
- Analysis of ATG10's role in cancer progression, metastasis, and therapeutic resistance.
- Identification of factors that modulate ATG10 activity.
Main Results
- ATG10 overexpression is linked to poor outcomes in endometrial, liver, leukemia, nasopharyngeal, gastric, and colorectal cancers.
- ATG10 promotes cancer progression by modulating epithelial-mesenchymal transition and cell cycle regulators (cyclin B1, CDK1, CDK2).
- ATG10 activity is inhibited by DDX10, PTBP1, sodium orthovanadate, podofilox, SIRT6, FAT1, SOX2, and specific microRNAs.
Conclusions
- ATG10 is a significant driver of cancer progression and metastasis across multiple malignancies.
- Targeting ATG10 presents a promising therapeutic avenue for cancer treatment.
- Further research into ATG10's regulatory mechanisms and inhibitors is warranted for clinical application.
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