Article
Oncology
Hao Zhou, Yichong Ning, Guirong Zeng, Chang Zhou, Xiaofeng Ding
Summary: Curcumin demonstrates strong cytotoxic activity against AML cells by modulating protein phosphorylation and protein-protein interaction network, leading to cell cycle arrest and apoptosis. It functions via inactivating AKT and synergizes with AKT inhibitor to suppress AML cell engraftment, proliferation, and survival in a xenograft mouse model.
Article
Endocrinology & Metabolism
Dongmei Hou, Qiang Ding, Ruiqi Li, Yuan Zhang, Fuming Zi
Summary: The aim of this study was to investigate the action and mechanism of metformin in acute myeloid leukemia (AML), in order to find cost-effective drugs for synergistic therapy to improve the survival rate of AML patients. The results showed that metformin inhibited AML cell proliferation, induced apoptosis, and arrested the cell cycle at the G0/G1 phase by inhibiting the PI3K/AKT/mTOR pathway.
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
(2023)
Article
Oncology
Wenwen Zhang, Qian Ma, Bing Long, Zhangyi Sun, Lingling Liu, Dongjun Lin, Minyi Zhao
Summary: In this study, it was found that RUNX3 is a super-enhancer-associated gene highly expressed in AML cells, and its high expression is associated with poor prognosis in AML patients. Knockdown of Runx3 significantly inhibits leukemia progression by inducing DNA damage and apoptosis.
FRONTIERS IN ONCOLOGY
(2021)
Article
Food Science & Technology
Ju-Huei Chien, Xiao-Fan Huang, Wen-Lin Lai, Kai-Fu Chang, Chia-Yu Li, Szu-Yin Chen, Chun-Yu Wu, Kuan-Ying Li, Nu-Man Tsai
Summary: This study revealed the anticancer potential of PPa extract in HL-60 cells by inhibiting cell proliferation through affecting cell cycle and inducing apoptosis. Moreover, PPa extract could modulate the expression of cell cycle-related proteins and activate apoptosis pathways, leading to cell death.
FOOD SCIENCE & NUTRITION
(2021)
Article
Biochemistry & Molecular Biology
Rania H. H. Abd El-Hameed, Mosaad S. S. Mohamed, Samir M. M. Awad, Bardes B. B. Hassan, Marwa Abd El-Fattah Khodair, Yara E. E. Mansour
Summary: A series of benzo[h]chromenes, benzo[f]chromenes, and benzo[h]chromeno[2,3-d]pyrimidines were synthesized and compounds 5a and 6a showed promising anti-cancer activity. These compounds suppressed cell growth in HL-60 by inducing cell cycle arrest and triggering cell apoptosis.
JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY
(2023)
Review
Oncology
Wonhyoung Seo, Prashanta Silwal, Ik-Chan Song, Eun-Kyeong Jo
Summary: In this review, the multifaceted functions of autophagy in AML were discussed, including its link to genetic alterations, potential prognostic predictors, and drivers of AML tumorigenesis. The crosstalk between autophagy and tumor cell metabolism and its impact on AML progression and treatment were also examined. Additionally, the potential therapeutics for AML, such as autophagy regulators, were described, along with their translation into clinical practice.
JOURNAL OF HEMATOLOGY & ONCOLOGY
(2022)
Article
Oncology
Tarang Gaur, Ramulu Poddutoori, Leena Khare, Bhausaheb Bagal, Sonal Rashmi, Nikhil Patkar, Prashant Tembhare, Subramanian Pg, Dhanlaxmi Shetty, Amit Dutt, Qi Zhang, Marina Konopleva, Uwe Platzbeckar, Sudeep Gupta, Susanta Samajdar, Murali Ramchandra, Navin Khattry, Syed K. Hasan
Summary: This study demonstrated that the CDK7 inhibitor XL102 can induce cell cycle arrest and apoptosis in acute myeloid leukemia (AML) cells through the CDK7/c-Myc/p53 axis. It also showed that XL102 has synergistic effects with Venetoclax in overcoming drug resistance. These findings highlight the potential of XL102 as a therapeutic option for AML.
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
(2023)
Article
Cell Biology
Chendi Xie, Hui Zhou, Dongmei Qin, Huijian Zheng, Yuanfang Tang, Wenjuan Li, Jie Zhou, Long Liu, Xinxin Yu, Hongpeng Duan, Yong Zhou, Zhifeng Li, Zhihong Fang, Yiming Luo, Bing Z. Carter, Bing Xu, Jie Zha
Summary: This study found that the combination of Bcl-2 inhibitor venetoclax and PPARa agonist chiglitazar can effectively eliminate LSCs of acute myeloid leukemia (AML) without damaging normal cells. This combination therapy also significantly inhibits AML progression in mouse models.
CELL DEATH & DISEASE
(2023)
Article
Oncology
You Jiang, Shui-Yan Wu, Yan-Ling Chen, Zi-Mu Zhang, Yan-Fang Tao, Yi Xie, Xin-Mei Liao, Xiao-Lu Li, Gen Li, Di Wu, Hai-Rong Wang, Ran Zuo, Hai-Bo Cao, Jing-Jing Pan, Juan-Juan Yu, Si-Qi Jia, Zheng Zhang, Xin-Ran Chu, Yong-Ping Zhang, Chen-xi Feng, Jian-Wei Wang, Shao-Yan Hu, Zhi-Heng Li, Jian Pan, Fang Fang, Jun Lu
Summary: This study systematically explored the molecular characteristics of CEBPG in AML and identified CEBPG as a potential therapeutic target for AML patients. It was found that CEBPG promotes AML cell proliferation by activating EIF4EBP1, thus contributing to the progression of AML.
CANCER CELL INTERNATIONAL
(2021)
Article
Oncology
Alec W. Stranahan, Iryna Berezniuk, Sohini Chakraborty, Faye Feller, Mona Khalaj, Christopher Y. Park
Summary: Acute myeloid leukemia (AML) is associated with high relapse rates and poor clinical outcomes. This study identifies ALOX5 as a resistance gene to anthracycline-based therapy in AML and suggests that inhibiting ALOX5 could enhance therapeutic efficacy in AML.
Article
Pathology
Shuyu Chen, Liang Zhong, Xuan Chu, Peng Wan, Zhenyan Liu, Yang Lu, Zhonghui Zhang, Xiao Wang, Ziwei Zhou, Xin Shao, Beizhong Liu
Summary: This study shows that overexpression of PLK4 is involved in tumorigenesis in acute myeloid leukemia (AML) by regulating cell cycle and inducing apoptosis. Inhibition of PLK4 leads to apoptosis, G2/M arrest, and endoplasmic reticulum stress in AML cells.
PATHOLOGY RESEARCH AND PRACTICE
(2023)
Article
Oncology
Majid Ghorbani, Mohammad Soukhtanloo, Amir Salek Farrokhi, Seyed Mahdi Hassanian, Fatemeh Ghorbani, Amir Reza Afshari, Mohsen Taherian, Mohammad Hadi Sadeghian
Summary: This research aimed to investigate the cytotoxic effects of Auraptene on HL60 and U937 cell lines. The results showed that Auraptene decreased cellular proliferation and induced oxidative stress in HL60 and U937 cells. Additionally, Auraptene induced cell cycle arrest and apoptosis by upregulating certain proteins. These findings suggest that Auraptene may be a promising anti-tumor agent against hematologic malignancies.
Article
Oncology
Xiangke Xin, Zheng Xu, Jia Wei, Yicheng Zhang
Summary: Metallothionein1X (MT1X) is highly expressed in acute myeloid leukemia (AML) and acts as a candidate prognostic indicator. Inhibiting MT1X can suppress AML cell proliferation, induce apoptosis, and inhibit nuclear factor-kappa B (NF-kappa B) signaling. MiR-376a-3p negatively regulates MT1X, suppressing AML cell proliferation and inducing apoptosis. These findings suggest that elevated MT1X expression may contribute to AML progression and indicate that the miR-376a/MT1X axis could be a potential therapeutic target for AML patients.
CANCER BIOLOGY & THERAPY
(2022)
Article
Oncology
Wen Zhang, Jingwen Liu, Yiming Li, Fujiang Guo
Summary: This study suggests that D36, a compound isolated from Psoralea corylifolia L., exhibits potential in treating acute myeloid leukemia (AML). D36 can induce cell death in AML cells through the activation of apoptosis and autophagy, as well as by blocking the cell cycle progression. Furthermore, D36 shows promising anti-tumor activity in a mouse model of AML without significant side effects.
CANCER CHEMOTHERAPY AND PHARMACOLOGY
(2022)
Editorial Material
Cell & Tissue Engineering
Malini Gupta, Britta Will
Summary: Adaptive aberrant gene regulation is a hallmark of malignant growth and therapy resistance in acute myeloid leukemia (AML). In this study, Eagle et al. identified oncogenic enhancer-driven overexpression of selenophosphate synthetase 2 (SEPHS2) as a targeted opportunity for mitigating malignant cell growth in AML.