Article
Cell Biology
Laura Mainz, Mohamed A. F. E. Sarhan, Sabine Roth, Ursula Sauer, Charis Kalogirou, Markus Eckstein, Elena Gerhard-Hartmann, Helen-Desiree Seibert, Hans-Ulrich Voelker, Carol Geppert, Andreas Rosenwald, Martin Eilers, Almut Schulze, Markus Diefenbacher, Mathias T. Rosenfeldt
Summary: The potential therapeutic target of macroautophagy/autophagy for various diseases, including cancer, is mainly based on preclinical mouse studies. This study introduces a shRNA transgenic mouse model that allows simultaneous knockdown of Atg7 in most organs, providing a valuable tool for further understanding of the role of autophagy impairment at different disease stages.
Article
Oncology
Ziva Frangez, Deborah Gerard, Zhaoyue He, Marios Gavriil, Yuniel Fernandez-Marrero, S. Morteza Seyed Jafari, Robert E. Hunger, Philippe Lucarelli, Shida Yousefi, Thomas Sauter, Lasse Sinkkonen, Hans-Uwe Simon
Summary: Research found significantly reduced expression of ATG5 and ATG7 in melanoma tissues, correlated with decreased autophagic activity and unfavorable clinical outcomes. NRF1 was identified to promote the production of ATG5 and ATG7, showing involvement in their regulation.
FRONTIERS IN ONCOLOGY
(2021)
Review
Cell Biology
Kaja Urbanska, Arkadiusz Orzechowski
Summary: While ATG5 and ATG7 were thought to be crucial for autophagy, recent research has revealed the existence of an alternative autophagy pathway independent of ATG5/ATG7. This alternative pathway differs in its molecular mechanism from the canonical pathway and may play a role in mitophagy. Further studies are needed to fully understand the function and significance of alternative autophagy in various cellular processes and disease pathogenesis.
Article
Biochemistry & Molecular Biology
Li Tan, Di Xiong, Hui Zhang, Sirou Xiao, Ruilan Yi, Jian Wu
Summary: Heart failure (HF) is a chronic disease characterized by inadequate blood and oxygen supply to peripheral tissues. This study investigated the mechanism of HF using H2O2-treated AC16 cells as a cellular model. The results showed that H2O2 stimulation increased the expression of ETS2, TUG1, and ATG7, while decreasing the expression of miR-129-5p. H2O2 stimulation also induced cardiomyocyte apoptosis and autophagy, which could be reversed by manipulating the ETS2/TUG1/miR-129-5p/ATG7 axis. Overall, these findings suggest that targeting this axis may provide new therapeutic options for treating HF.
Article
Cell Biology
Nemanja Vujic, Ivan Bradic, Madeleine Goeritzer, Katharina B. Kuentzel, Silvia Rainer, Dagmar Kratky, Branislav Radovic
Summary: The study shows that loss of ATG5 results in depletion of LC3-II, while loss of ATG7 has no significant impact on LC3-PE conjugation. The level of LC3 lipidation in macrophages under inflammatory stimuli is determined by their metabolic status, with ATG7 playing a supportive but nonessential role.
Article
Biochemistry & Molecular Biology
Andrea Barrientos-Riosalido, Monica Real, Laia Bertran, Carmen Aguilar, Salome Martinez, David Parada, Margarita Vives, Fatima Sabench, David Riesco, Daniel Del Castillo, Cristobal Richart, Teresa Auguet
Summary: This study analyzed the expression of ATG7 gene in obesity-associated NAFLD and found that ATG7 was highly expressed in NASH patients. ATG7 may play an important role in the pathogenesis of NAFLD, especially in NASH, possibly having a protective effect.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Oncology
Dalyia N. Benjamin, Tracey R. O'Donovan, Kristian B. Laursen, Nina Orfali, Mary R. Cahill, Nigel P. Mongan, Lorraine J. Gudas, Sharon L. McKenna
Summary: This study investigates the potential of promoting cell differentiation in ATRA resistant AML cells by assessing the role of autophagy induction with valproic acid. The results suggest that the combination of ATRA and valproic acid can enhance autophagy and promote differentiation in both ATRA-sensitive and -resistant cell lines, indicating the importance of autophagy in the treatment.
FRONTIERS IN ONCOLOGY
(2022)
Article
Multidisciplinary Sciences
Jaclyn S. Long, Elzbieta Kania, David G. McEwan, Valentin J. A. Barthet, Martina Brucoli, Marcus J. G. W. Ladds, Christoph Nossing, Kevin M. Ryan
Summary: Research findings show that the loss of Atg7 in a model of PDAC with mutant Kras(G12D) and mutant Trp53(172H/+) promotes tumor development and enhances metastasis, while reducing the occurrence of metastasis. Tumors with Atg7(+/-) have lower levels of succinate and lower invasion capabilities.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Editorial Material
Cell Biology
Jack J. Collier, Monika Olahova, Thomas G. McWilliams, Robert W. Taylor
Summary: ATG7 plays a crucial role in autophagy, and dysfunction of ATG7 may lead to neurological issues. Studies have identified patients with specific ATG7 variants suffering from neurodevelopmental disorders, with the pathology being linked to attenuated autophagy.
Article
Critical Care Medicine
Jian Jin, Kai-si Zhu, Shu-min Tang, Yang Xiang, Ming-yi Mao, Xu-dong Hong, Ai-fen Chen, Xu-dong Zhang, Hao Lu, Zheng-li Chen, Jin-fang Wu, Sun-feng Pan, Shi-hui Zhu
Summary: Trehalose reduces stress-induced wound tissue damage by promoting cell proliferation and migration, reducing necrosis and apoptosis, thus promoting wound healing.
Article
Cardiac & Cardiovascular Systems
Yong Wang, Xiaoguang Lu, Xiaoping Wang, Qi Qiu, Ping Zhu, Lin Ma, Xiao Ma, Joerg Herrmann, Xueying Lin, Wei Wang, Xiaolei Xu
Summary: The study aimed to elucidate the dynamic autophagic defects in AIC and identify a mechanism-based therapy through genetic and pharmacological studies. Results showed that atg7-based autophagy activation is an effective therapeutic avenue to reverse the decline in cardiac function in AIC, highlighting the time-dependent nature of autophagy-based therapy.
CIRCULATION RESEARCH
(2021)
Article
Cell Biology
Bora Lee, Hyejin Shin, Ji-Eun Oh, Jaekyoung Park, Mira Park, Seung Chel Yang, Jin-Hyun Jun, Seok-Ho Hong, Haengseok Song, Hyunjung Jade Lim
Summary: The study revealed that the deficit of autophagy in the uterine vessel microenvironment provokes hyperpermeability through the deregulation of VEGFA, NOS1, and CTNNB1, affecting the vascular stability and function.
Article
Biochemistry & Molecular Biology
Jian Zhang, Peiyan Wang, Miao Song, Xuliang Zhang, Siming Huo, Jiayu Du, Bo Li, Zheng Cao, Yanfei Li
Summary: The present study investigated the effect of T-2 toxin on osteoblast differentiation and mineralization by treating MC3T3-E1 cells with different concentrations of T-2 toxin. The results showed that T-2 toxin at 4 and 8 nM significantly inhibited cell viability and impaired osteoblastic differentiation and mineralization. The activation of the Wnt signaling pathway mitigated the T-2 toxin-induced damage, while the inhibition of autophagy exacerbated it. Our findings also revealed a positive feedback loop between the Wnt signaling pathway and autophagy.
CHEMICO-BIOLOGICAL INTERACTIONS
(2023)
Review
Medicine, Research & Experimental
Jack J. Collier, Fumi Suomi, Monika Olahova, Thomas G. McWilliams, Robert W. Taylor
Summary: ATG proteins are essential for macroautophagy and play important roles beyond autophagic elimination. Dysfunction of ATG7 is associated with diseases, but the mechanisms of how it contributes to these diseases remain unclear. Further research on the relationship between ATG7 dysfunction and diseases will help develop therapies for disorders involving ATG7 deficiency and impaired autophagy.
EMBO MOLECULAR MEDICINE
(2021)
Article
Pharmacology & Pharmacy
Hu-Qiang He, Yuan-Qing Qu, Betty Yuen Kwan Law, Cong-Ling Qiu, Yu Han, Ivo Ricardo de Seabra Rodrigues Dias, Yong Liu, Jie Zhang, An-Guo Wu, Cheng-Wen Wu, Simon Wing Fai Mok, Xin Cheng, Yan-Zheng He, Vincent Kam Wai Wong
Summary: The study found that calcification was upregulated in HASMCs treated with AGEs when autophagy and apoptosis were activated. However, AGEs-activated calcification and apoptosis were suppressed in Atg7 knockout cells or pretreated with wortmannin (WM), an autophagy inhibitor. This suggests potential clinical applications for autophagy inhibitors in the treatment of diabetes-related vascular calcification.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Cell Biology
Ke Mi, Lizhong Zeng, Yang Chen, Jingya Ning, Siyuan Zhang, Peilin Zhao, Shuanying Yang
Summary: In this study, the researchers explored the role of DHX38 in NSCLC and its underlying molecular mechanism. They found that DHX38 was overexpressed in NSCLC and patients with high DHX38 expression had poor prognosis. DHX38 promoted cell proliferation, migration, and invasion in NSCLC and activated the MAPK pathway. The researchers also identified G3BP1 as a target protein that interacted with DHX38 and showed that DHX38 regulated the expression of G3BP1. Silencing G3BP1 reversed the effects of DHX38 overexpression on tumor cell proliferation, migration, and invasion and inhibited the MAPK pathway activation.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Tiina A. Jokela, Mark A. Dane, Rebecca L. Smith, Kaylyn L. Devlin, Sundus Shalabi, Jennifer C. Lopez, Masaru Miyano, Martha R. Stampfer, James E. Korkola, Joe W. Gray, Laura M. Heiser, Mark A. Labarge
Summary: Microenvironment signals have a significant impact on cell fate and tissue homeostasis. Understanding how different microenvironment factors regulate cellular phenotype has been challenging. In this study, a high-throughput microenvironment microarray was used to identify factors that support the proliferation and maintenance of primary human mammary luminal epithelial cells. Multiple factors that modulate luminal cell number were identified and their effects were confirmed using RNA sequencing and cell-based functional studies. Hepatocyte growth factor (HGF) was found to be robust to individual variation and played a role in expanding luminal cells. Our approach demonstrates the power of high-dimensional cell-based approaches in dissecting microenvironmental signals.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chao He, Yongfeng Ding, Yan Yang, Gang Che, Fei Teng, Haohao Wang, Jing Zhang, Donghui Zhou, Yanyan Chen, Zhan Zhou, Haiyong Wang, Lisong Teng
Summary: This study categorized gastric cancer patients into three stemness subtypes, each demonstrating distinct prognoses, components of tumor microenvironment (TME) infiltration, and varying sensitivity or resistance to treatment. A stemness risk model was constructed to predict treatment response and prognosis.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haile Zhao, Lijuan Feng, Rui Cheng, Man Wu, Xiaozhou Bai, Lifei Fan, Yaping Liu
Summary: miR-29c-3p is overexpressed in benign and malignant ovarian carcinoma and is associated with poor prognosis. Its overexpression modulates tumorigenesis in ovarian cancer cells, including epithelial-mesenchymal transition, proliferation, migration, and invasion, through the regulation of DNMT3A, TET1, and HBP1. miR-29c-3p may serve as a potential biomarker for clinical diagnosis or co-diagnosis of ovarian carcinoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haiyan Zhao, Fangfang Bi, Mengyuan Li, Yuhan Diao, Chen Zhang
Summary: This study confirmed the tumor suppressor effect of RNF180 on ovarian cancer, elucidated the mechanism of the molecule network related to RNF180 and IPO4 in ovarian cancer, and identified a new therapeutic target for ovarian cancer.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chu Chen, Guanhua Xu, Jiajia Chen, Chunshuai Wu, Jinlong Zhang, Jiawei Jiang, Hongxiang Hong, Zhiming Cui
Summary: This study investigated the role of transcription factor FoxO1 in facet joint osteoarthritis (FJOA) and found that FoxO1 deletion led to severe osteoarthritic changes. Transcriptome sequencing and bioinformatics analysis identified differentially expressed genes (DEGs) and potential key contributors to FJOA. Additionally, over-expression of certain genes and inhibition of others were shown to counteract the impairments caused by FoxO1 deletion in chondrocyte migration and extracellular matrix synthesis. These findings help unravel the molecular mechanisms underlying FJOA and open up promising therapeutic avenues for its treatment.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Wen Deng, Ru Chen, Situ Xiong, Jianqiang Nie, Hailang Yang, Ming Jiang, Bing Hu, Xiaoqiang Liu, Bin Fu
Summary: This study demonstrates that circFSCN1 is upregulated in bladder cancer and associated with cancer-specific survival. CircFSCN1 promotes tumor progression and epithelial-mesenchymal transition in bladder cancer through enhancing MDM2-mediated silencing of p53 by sponging miR-145-5p.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Jun Wu, Weibin Hu, Wenhui Yang, Yihao Long, Kaizhao Chen, Fugui Li, Xiaodong Ma, Xun Li
Summary: Cholesterol biosynthesis and metabolism play critical roles in tumor development and microenvironmental conditions. Squalene Epoxidase (SQLE), the second rate-limiting enzyme in cholesterol synthesis, is found to be uniquely expressed in various cancers, and its expression level is closely associated with tumor mutation burden and microsatellite instability. SQLE expression is negatively correlated with immune cell infiltration. Inhibition of SQLE alters the immune response in the tumor microenvironment. Furthermore, protein metabolism and translation are identified as main binding factors with SQLE.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhihong Zhang, Mingyue Li, Yi Tai, Yue Xing, Hongxiang Zuo, Xuejun Jin, Juan Ma
Summary: ZNF70 plays an important role in colitis-associated colorectal cancer (CAC) by regulating macrophages IL-1 beta secretion to promote HCT116 proliferation. It may serve as a promising target for treating CAC.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zenghong Wu, Gangping Li, Weijun Wang, Kun Zhang, Mengke Fan, Yu Jin, Rong Lin
Summary: This study comprehensively explored the role of immune checkpoints and tumor microenvironment in gastric cancer patients based on genomic data. It constructed an ICIs signature and ICI score to evaluate patient prognosis and heterogeneity.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Yantong Wan, Jieshu Zhou, Panpan Zhang, Xuemei Lin, Hao Li
Summary: This study found that Rac1 plays a role in astrocyte activation and attenuates chronic inflammatory pain by blocking the phosphorylation of NLRP3 inflammasome and NF-kappa B.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhen Wang, Diankun She, Lei Liu, Xianming Hua, Hao Zhu, Lingfeng Yu, Han Wang, Yan Zhu, Gentao Fan, Yicun Wang, Meng Xu, Guangxin Zhou
Summary: Circular RNAs (circRNAs) are non-coding RNAs that play a role in the regulation of various cancers, including osteosarcoma (OS). This study identified circSATB2 as a highly expressed circRNA in OS tissues and cell lines, and demonstrated its involvement in promoting OS proliferation and migration. Mechanistically, circSATB2 was found to regulate the progression of OS by sponging miR-661 and FUS to regulate ZNFX1 mRNA. These findings suggest that circSATB2 could serve as a prognostic marker and therapeutic target for osteosarcoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Kenichi Ogata, Masafumi Moriyama, Tatsuya Kawado, Hiroki Yoshioka, Aiko Yano, Mayu Matsumura-Kawashima, Seiji Nakamura, Shintaro Kawano
Summary: This study found that extracellular vesicles released by induced pluripotent stem cells can reduce inflammatory cell infiltration, increase saliva volume, and decrease the production of antibodies associated with Sjogren's syndrome in a mouse model. The let-7 family in these vesicles may suppress the expression of TLR4 and NF-kappa B, which leads to the inhibition of pro-inflammatory cytokine production through the MAPK pathway.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Mikayla R. Erdelsky, Sarah A. Groves, Charmi Shah, Samantha B. Delios, M. Bibiana Umana, Donald H. Maurice
Summary: Recent evidence suggests that cAMP signaling within the primary cilium plays a crucial role in promoting adipogenic differentiation of 3T3-L1 preadipocytes. In this study, the researchers identified the specific cAMP phosphodiesterases expressed by these cells and found that inhibition of PDE4 promotes FFAR4-mediated adipogenesis. This work could potentially lead to the discovery of more targeted therapeutic approaches for controlling adipogenesis and differentiation of other stem cells.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chun-Hui Liu, Jun-Jie Zhang, Qian-Jin Zhang, Yang Dong, Zhen-Duo Shi, Si-Hao Hong, Hou-Guang He, Wei Wu, Cong-Hui Han, Lin Hao
Summary: Bladder cancer, the most common malignant tumor in the urinary system, is associated with significantly up-regulated expression of P3H4, which is regulated by METTL3 and plays a crucial role in the proliferation, metastasis, and EMT progression of bladder cancer. Targeting this METTL3-P3H4 pathway may serve as a potential therapeutic strategy for bladder cancer.
CELLULAR SIGNALLING
(2024)