Article
Cell Biology
Emir Bozkurt, Heiko Dussmann, Manuela Salvucci, Brenton L. Cavanagh, Sandra Van Schaeybroeck, Daniel B. Longley, Seamus J. Martin, Jochen H. M. Prehn
Summary: The study reveals that TRAIL signaling not only activates apoptosis in colon cancer cells but also induces entosis through TRAIL receptors and the structural presence of caspase-8. The association of TRAIL signaling with cell-in-cell structures is significant in colorectal cancer, especially in the context of patient prognosis. Factors controlling entosis in tumors remain to be elucidated despite the evidence of entosis in cancers.
JOURNAL OF CELL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Chiara Musiu, Simone Caligola, Alessandra Fiore, Alessia Lamolinara, Cristina Frusteri, Francesco Domenico Del Pizzo, Francesco De Sanctis, Stefania Cane, Annalisa Adamo, Francesca Hofer, Roza Maria Barouni, Andrea Grilli, Serena Zilio, Paolo Serafini, Evelina Tacconelli, Katia Donadello, Leonardo Gottin, Enrico Polati, Domenico Girelli, Ildo Polidoro, Piera Amelia Iezzi, Domenico Angelucci, Andrea Capece, Ying Chen, Zheng-Li Shi, Peter J. Murray, Marco Chilosi, Ido Amit, Silvio Bicciato, Manuela Iezzi, Vincenzo Bronte, Stefano Ugel
Summary: Research has shown that FLIP can control cytokine release syndrome (CRS) by activating a STAT3-dependent inflammatory program. Expression of a viral FLIP homolog in myeloid cells can trigger a fatal inflammatory syndrome in mice, characterized by increased cytokine output, lymphopenia, lung injury, and multiple organ dysfunctions. Targeting the STAT3 pathway may help alleviate inflammation, immune disorders, and organ failures associated with CRS.
CELL DEATH AND DIFFERENTIATION
(2022)
Article
Environmental Sciences
Haojie Li, Junjiang Fan, Yangfei Zhao, Jiarong Yang, Huimiao Xu, Ram Kumar Manthari, Xiaofang Cheng, Jundong Wang, Jinming Wang
Summary: The study shows that long-term excessive intake of fluoride can cause kidney damage and apoptosis, while dietary calcium supplementation can alleviate this damage. Calcium supplementation mitigates fluoride-induced kidney apoptosis through various signaling pathways.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2021)
Article
Biochemistry & Molecular Biology
Zifei Han, Zihao Li, Radhika Raveendran, Shegufta Farazi, Cheng Cao, Robert Chapman, Martina H. Stenzel
Summary: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in cancer cells, but its clinical development is hindered by its short circulation half-life. Researchers have developed core-cross-linked micelles that successfully induce apoptosis in colon cancer cells, offering a potential alternative to TRAIL.
Article
Oncology
Nagamani Vunnam, Malaney C. Young, Elly E. Liao, Chih Hung Lo, Evan Huber, MaryJane Been, David D. Thomas, Jonathan N. Sachs
Summary: Although nimesulide has been taken off the market due to hepatotoxicity, it is still used as a valuable research tool for developing new anticancer drugs. Several studies have been conducted to modify its structure and develop more potent anticancer agents. Understanding the mechanism of action for nimesulide is crucial in realizing its potential.
CANCER BIOLOGY & THERAPY
(2023)
Article
Biochemistry & Molecular Biology
Lei Chen, Miao Hao, Jingmin Yan, Lin Sun, Guihua Tai, Hairong Cheng, Yifa Zhou
Summary: The active compound DHCP isolated from heat-treated citrus pectin induces cell death in colon cancer cells by inducing mitochondrial ROS, enhances cancer cells sensitivity to TRAIL, and synergistically inhibits the growth of HCT116 and HT-29 xenografts. Furthermore, DHCP increases DR5 expression to further inhibit tumor growth.
JOURNAL OF BIOLOGICAL CHEMISTRY
(2021)
Article
Oncology
Miao He, Yingying He, Jian Xu, Youcai Zhang, Xiaoyu Cao, Li Wang, Feng Luo
Summary: This study revealed the association between FADD expression and prognosis, immune exhaustion, and tumor malignancy in LUAD patients. In addition, FADD can serve as an efficient indicator for assessing sensitivity to chemotherapy and immunotherapy, making it a potential new target for precision medicine and targeted therapy for LUAD.
FRONTIERS IN ONCOLOGY
(2023)
Article
Multidisciplinary Sciences
Yosuke Tanaka, Reina Takeda, Tsuyoshi Fukushima, Keiko Mikami, Shun Tsuchiya, Moe Tamura, Keito Adachi, Terumasa Umemoto, Shuhei Asada, Naoki Watanabe, Soji Morishita, Misa Imai, Masayoshi Nagata, Marito Araki, Hitoshi Takizawa, Tomofusa Fukuyama, Chrystelle Lamagna, Esteban S. Masuda, Ryoji Ito, Susumu Goyama, Norio Komatsu, Tomoiku Takaku, Toshio Kitamura
Summary: Leukemia stem cells in chronic myeloid leukemia are resistant to imatinib, but can be eliminated by combining imatinib with IRAK1/4 inhibitors that inhibit the IRAK1/4-NF-kappa B-PD-L1 signaling pathway.
NATURE COMMUNICATIONS
(2022)
Article
Pharmacology & Pharmacy
Chantana Boonyarat, Chavi Yenjai, Prasert Reubroycharoen, Suchada Chaiwiwatrakul, Pitchayakarn Takomthong, Pongput Pimsa, Pornthip Waiwut
Summary: This study investigated the mechanisms behind TRAIL-induced HT29 colon cancer cell death by using heptaphylline and 7-methoxyheptaphylline from Clausena harmandiana. The findings showed that 7-methoxyheptaphylline enhanced the expression of death receptor 5 (DR5) via the JNK pathway, resulting in intensified TRAIL-induced HT29 cell death.
BIOLOGICAL & PHARMACEUTICAL BULLETIN
(2023)
Article
Health Care Sciences & Services
Shimin Xu, Yuezhong Li, Junshan Zhang, Zhiwei Li, Yanping Xing
Summary: The study discovered that miR-98 inhibits apoptosis of nucleus pulposus cells by targeting TRAIL, thereby providing a potential therapeutic target for cervical intervertebral disc degeneration.
JOURNAL OF HEALTHCARE ENGINEERING
(2022)
Article
Oncology
Darren C. Phillips, Fritz G. Buchanan, Dong Cheng, Larry R. Solomon, Yu Xiao, John Xue, Stephen K. Tahir, Morey L. Smith, Haichao Zhang, Deborah Widomski, Vivek C. Abraham, Nan Xu, Zhihong Liu, Li Zhou, Enrico DiGiammarino, Xin Lu, Nandini Rudra-Ganguly, Bruce Trela, Susan E. Morgan-Lappe
Summary: This study highlights the activity of a hexavalent TRAIL-receptor agonistic fusion protein in preclinical models of solid tumors, distinguishing it mechanistically from other TRAIL-based therapeutics.
Article
Biochemistry & Molecular Biology
Yana Vladimirovna Lomovskaya, Margarita Igorevna Kobyakova, Anatoly Sergeevich Senotov, Alexey Igorevich Lomovsky, Vladislav Valentinovich Minaychev, Irina Sergeevna Fadeeva, Daria Yuryevna Shtatnova, Kirill Sergeevich Krasnov, Alena Igorevna Zvyagina, Vladimir Semenovich Akatov, Roman Sergeevich Fadeev
Summary: The resistance of leukemic cells to TRAIL-induced apoptosis is a major challenge in the treatment of leukemia. In this study, researchers discovered that human acute myeloid leukemia cells, when subjected to high-density culture conditions, displayed a macrophage-like phenotype and increased resistance to TRAIL-induced cell death. This resistance can be attributed to a decrease in the expression of death receptors DR4 and DR5 on the leukemic cells. The findings suggest that stress conditions in high-density cell cultures may contribute to tumor progression by promoting TRAIL resistance.
Article
Cell Biology
Rosario Yerbes, Rocio Mora-Molina, F. Javier Fernandez-Farran, Laura Hiraldo, Abelardo Lopez-Rivas, Carmen Palacios
Summary: This study reveals a previously unknown cell death mechanism triggered in glutamine-addicted tumor cells in response to glutamine metabolism limitation. The mechanism is regulated by GCN2 activation induced by glutamine starvation and involves the activation of the extrinsic apoptotic pathway mediated by TRAIL-R2.
CELL DEATH & DISEASE
(2022)
Article
Multidisciplinary Sciences
Jing Liu, Collin Tokheim, Jonathan D. Lee, Wenjian Gan, Brian J. North, X. Shirley Liu, Pier Paolo Pandolfi, Wenyi Wei
Summary: Genetic fusions affecting degrons can alter protein stability and increase oncogene stability. Recurrent fusions such as BCR-ABL, CCDC6-RET, and PML-RARA disrupt protein stability by exchanging internal degrons. Additionally, fusions like EGFR or RAF1 can be stabilized by losing a C-terminal degron.
NATURE COMMUNICATIONS
(2021)
Article
Oncology
K. M. A. Zinnah, Sang-Youel Park
Summary: The study demonstrated the mechanism behind the synergistic anticancer effect of amitriptyline and TRAIL, showing that amitriptyline increases TRAIL-induced apoptosis by upregulating death receptors DR4 and DR5. Inhibition of autophagy by amitriptyline was also shown to enhance DR4 and DR5 expression.