Article
Environmental Sciences
Yue Wu, Ruijie Lu, Yujie Lin, Jinjin Wang, Zijian Lou, Xiaochun Zheng, Ling Zhang, Ruolang Pan, Gang Lu, Qingxia Fang
Summary: In this study, we found that long-term exposure to DEHP, an EDCs and plasticizer, is significantly associated with increased risks of various human diseases, including colorectal cancer. Our findings suggest that DEHP can trigger metabolic reprogramming in colorectal cancer cells, promoting cell growth and reducing sensitivity to 5-FU. Mechanistic studies showed that DEHP decreases glycolysis and increases OXPHOS in SW620 cells. In vivo experiments further demonstrated that DEHP promotes tumorigenic progression and decreases survival time in mice. Overall, our study highlights the potential risk of DEHP in colorectal cancer development.
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
(2023)
Review
Oncology
Fahim Ahmad, Murali Krishna Cherukuri, Peter L. Choyke
Summary: While low-risk localized prostate cancer has a good prognosis with effective treatments, metastatic prostate cancer remains incurable and treatment resistance is a major issue. Resistance is primarily driven by tumor heterogeneity, altered genetic signatures, and metabolic reprogramming enabling tumors to adapt to drugs. Understanding prostate cancer metabolism may offer insights into therapy-induced adaptive responses and more durable therapeutic outcomes.
BRITISH JOURNAL OF CANCER
(2021)
Review
Biochemistry & Molecular Biology
Francesco Lasorsa, Nicola Antonio di Meo, Monica Rutigliano, Matteo Ferro, Daniela Terracciano, Octavian Sabin Tataru, Michele Battaglia, Pasquale Ditonno, Giuseppe Lucarelli
Summary: Prostate cancer is a common malignancy in men and a leading cause of cancer death. The cancer cells have specific metabolic characteristics, including increased lipogenesis, cholesterogenesis, and reliance on glutamine. The tumor microenvironment also plays a role in cancer progression through interactions between cancer and stromal cells. The use of multi-omic approaches can provide a comprehensive understanding of the metabolic changes in prostate cancer.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biotechnology & Applied Microbiology
Zhenzhou Xu, Liang Huang, Tao Dai, Xiaming Pei, Longzheng Xia, Gongqian Zeng, Mingji Ye, Kan Liu, Fuhua Zeng, Weiqing Han, Shusuan Jiang
Summary: This study demonstrated that increased expression of SQLE in CRPC cells plays a role in mediating castration resistance by regulating metabolic reprogramming. Silencing SQLE restored sensitivity to drug-resistant cells and reduced lymph node metastasis by inhibiting fatty acid oxidation. Specific inhibitors of SQLE were also shown to enhance sensitivity of prostate cancer cells to drugs.
ONCOTARGETS AND THERAPY
(2021)
Article
Oncology
Simona Nanni, Aurora Aiello, Chiara Salis, Agnese Re, Chiara Cencioni, Lorenza Bacci, Francesco Pierconti, Francesco Pinto, Cristian Ripoli, Paola Ostano, Silvia Baroni, Giacomo Lazzarino, Barbara Tavazzi, Dario Pugliese, PierFrancesco Bassi, Claudio Grassi, Simona Panunzi, Giovanna Chiorino, Alfredo Pontecorvi, Carlo Gaetano, Antonella Farsetti
Summary: The study revealed the significant role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in prostate cancer metabolism, with its silencing causing metabolic reprogramming and reverting the phenotype of prostate cancer cells to that of normal prostate cells.
Article
Biochemistry & Molecular Biology
Sarah Krantz, Young-Mee Kim, Shubhi Srivastava, Joseph W. Leasure, Peter T. Toth, Glenn Marsboom, Jalees Rehman
Summary: Research has shown that there is mitophagy and mitochondrial biogenesis during the differentiation of pluripotent stem cells, impacting metabolic rewiring and increased oxidative metabolism of the cells. During endothelial cell differentiation, mitophagy initiates an increase in mitochondrial biogenesis and oxidative metabolism through transcriptional changes.
JOURNAL OF BIOLOGICAL CHEMISTRY
(2021)
Review
Medicine, Research & Experimental
Hong Xiang, Runjuan Yang, Jiaxin Tu, Yan Xi, Shilei Yang, Linlin Lv, Xiaohan Zhai, Yanna Zhu, Deshi Dong, Xufeng Tao
Summary: Abnormal intracellular metabolism in pancreatic cancer not only provides nutrition for tumor development, but also affects the function of immune cells in the immune microenvironment, promoting immune escape. This review discusses the emerging role of immune cells in pancreatic cancer, focusing on metabolic reprogramming and key metabolic pathways. The hotspots of immune cell metabolic reprogramming in pancreatic cancer mainly involve glucose metabolism, lipid metabolism, tricarboxylic acid cycle, and amino acid metabolism, which impact the function of anti-tumor immune cells and immunosuppressive cells through key metabolic signaling pathways. The review also elaborates on drugs targeting tumor metabolism pathways for clinical treatment of pancreatic cancer.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Biochemistry & Molecular Biology
Suryakant Niture, Minghui Lin, Joab O. Odera, John Moore, Hong Zhe, Xiaoxin Chen, Simeng Suy, Sean P. Collins, Deepak Kumar
Summary: TNFAIP8 promotes prostate cancer progression by enhancing cell metabolic activities and survival through regulating oxidative phosphorylation and glycolysis. It increases glucose consumption and ATP production by regulating the expression of glucose metabolizing enzymes in PCa cells. Additionally, TNFAIP8 modulates glycolytic metabolites production and maintains mitochondrial membrane potential, indicating its potential as a biomarker and therapeutic target for prostate cancer.
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
(2021)
Review
Oncology
Martina Addeo, Giuseppina Di Paola, Henu Kumar Verma, Simona Laurino, Sabino Russi, Pietro Zoppoli, Geppino Falco, Pellegrino Mazzone
Summary: Gastric cancer stem cells play a crucial role in the initiation and progression of gastric cancer, with features like self-renewal capability and resistance to current anticancer therapies. Targeting metabolic pathways of cancer stem cells could be a promising strategy in cancer therapy.
FRONTIERS IN ONCOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Wenjuan Wang, Aihua Zhang
Summary: Arsenic is a common environmental pollutant that can cause damage to multiple systems and organs in the body. The lungs are particularly sensitive to arsenic exposure, and respiratory disease is thought to be the leading cause of death from arsenic poisoning. This study found that HIF-1 alpha plays a key role in arsenic-induced lung injury.
BIOLOGICAL TRACE ELEMENT RESEARCH
(2022)
Article
Pathology
Agnese Orsatti, Maria Sirolli, Francesca Ambrosi, Tania Franceschini, Francesca Giunchi, Eugenia Franchini, Marco Grillini, Francesco Massari, Veronica Mollica, Federico Mineo Bianchi, Maurizio Colecchia, Michelangelo Fiorentino, Costantino Ricci
Summary: This study found differential expression and modulation of SOX2 and PRAME during the reprogramming of germ cell tumors, supporting a complex pathogenetic model where the interactions between these two molecules are crucial in determining the fate of GCTT.
PATHOLOGY RESEARCH AND PRACTICE
(2022)
Article
Biochemistry & Molecular Biology
Mengnan Hu, Ruoxuan Bao, Miao Lin, Xiao-Ran Han, Ying-Jie Ai, Yun Gao, Kun-Liang Guan, Yue Xiong, Hai-Xin Yuan
Summary: In this study, a novel association between ALK and PFKFB3 was discovered, and it was demonstrated that ALK promotes PFKFB3 transcription through STAT3 to enhance cell proliferation and tumorigenesis, providing an alternative strategy for the treatment of ALK-positive tumors.
Review
Medicine, Research & Experimental
Zhenzhen Li, Chanjun Sun, Zhihai Qin
Summary: Cancer cells adapt their metabolism to proliferate and survive in harsh environments, with a close relationship between tumor microenvironment and cancer-associated fibroblasts (CAFs) playing key roles in tumor growth and metastasis. CAFs act as major regulators in shaping tumor metabolism, especially through dysregulation of metabolic pathways, influencing cancer cell behavior and response to therapy. The interaction and crosstalk between cancer cells and CAFs contribute to metabolic reprogramming that impacts cancer cell growth and progression.
Article
Public, Environmental & Occupational Health
Renli Ning, Yulei Pei, Ping Li, Wei Hu, Yong Deng, Zhengshan Hong, Yun Sun, Qing Zhang, Xiaomao Guo
Summary: This study monitored 1,701 metabolites and found a change in urine metabolite profiles in PCa patients following CIRT. 35 significantly altered metabolites were identified, with most of them being amino acids. The arginine biosynthesis and histidine metabolism pathways were the most significantly altered pathways. Hierarchical cluster analysis showed that patients could be grouped into two categories based on their metabolite profiles after CIRT. The arginine biosynthesis and phenylalanine, tyrosine, and tryptophan biosynthesis pathways were the most discriminated pathways.
FRONTIERS IN PUBLIC HEALTH
(2021)
Article
Biochemistry & Molecular Biology
Shashi Anand, Mohammad Aslam Khan, Haseeb Zubair, Sarabjeet Kour Sudan, Kunwar Somesh Vikramdeo, Sachin Kumar Deshmukh, Shafquat Azim, Sanjeev Kumar Srivastava, Seema Singh, Ajay Pratap Singh
Summary: Extensive desmoplasia and poor vasculature contribute to the aggressiveness and therapy resistance of pancreatic tumors by causing severe hypoxia. In this study, we identify the HuR/MYB/HIF1 alpha axis as a critical regulator of the metabolic plasticity and hypoxic survival of pancreatic cancer cells. HuR translocates from the nuclear to the cytoplasm under hypoxia and stabilizes MYB transcripts, which in turn upregulates HIF1 alpha transcriptionally. MYB promotes the transcription of multiple HIF1 alpha-regulated glycolytic genes by binding directly to their promoters, thus enhancing HIF1 alpha recruitment to hypoxia-responsive elements through interaction with p300-dependent histone acetylation. Depletion of MYB significantly reduces tumorigenic ability, glucose uptake, and metabolism in orthotopic mouse models of pancreatic cancer, even after the restoration of HIF1 alpha. These findings highlight the essential role of MYB in the metabolic reprogramming that supports the survival of pancreatic cancer cells under hypoxia.
Article
Pathology
Jordan E. Vellky, Emily A. Ricke, Wei Huang, William A. Ricke
Summary: Distinguishing between indolent and aggressive prostate cancers is crucial for optimal treatment. The nucleolar protein BOP1, previously associated with other cancers, was found to have increased expression and cytoplasmic localization in advanced stages of CaP. Furthermore, genetic knockdown of BOP1 in metastatic CaP models resulted in decreased proliferation and motility, pointing to a potential prognostic significance and functional role of BOP1 in advanced CaP.
AMERICAN JOURNAL OF PATHOLOGY
(2021)
Article
Multidisciplinary Sciences
Yuanyuan Qiao, Xiao-Ming Wang, Rahul Mannan, Sethuramasundaram Pitchiaya, Yuping Zhang, Jesse W. Wotring, Lanbo Xiao, Dan R. Robinson, Yi-Mi Wu, Jean Ching-Yi Tien, Xuhong Cao, Stephanie A. Simko, Ingrid J. Apel, Pushpinder Bawa, Steven Kregel, Sathiya P. Narayanan, Gregory Raskind, Stephanie J. Ellison, Abhijit Parolia, Sylvia Zelenka-Wang, Lisa McMurry, Fengyun Su, Rui Wang, Yunhui Cheng, Andrew D. Delekta, Zejie Mei, Carla D. Pretto, Shaomeng Wang, Rohit Mehra, Jonathan Z. Sexton, Arul M. Chinnaiyan
Summary: Research has shown that androgens regulate the expression of ACE2, TMPRSS2, and AR in lung epithelial cells, affecting the risk of COVID-19 infection in males over 70 years old. The use of AR or BET antagonists can inhibit SARS-CoV-2 infection, providing support for further investigation into transcriptional inhibition for the treatment or prevention of COVID-19.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Correction
Biochemistry & Molecular Biology
Larischa de Wet, Anthony Williams, Marc Gillard, Steven Kregel, Sophia Lamperis, Lisa C. Gutgesell, Jordan E. Vellky, Ryan Brown, Kelly Conger, Gladell P. Paner, Heng Wang, Elizabeth A. Platz, Angelo M. De Marzo, Ping Mu, Jonathan L. Coloff, Russell Z. Szmulewitz, Donald J. Vander Griend
Article
Biology
Justin H. Hwang, Rand Arafeh, Ji-Heui Seo, Sylvan C. Baca, Megan Ludwig, Taylor E. Arnoff, Lydia Sawyer, Camden Richter, Sydney Tape, Hannah E. Bergom, Sean McSweeney, Jonathan P. Rennhack, Sarah A. Klingenberg, Alexander T. M. Cheung, Jason Kwon, Jonathan So, Steven Kregel, Eliezer M. Van Allen, Justin M. Drake, Matthew L. Freedman, William C. Hahn
Summary: The study reveals the physical interactions between CREB5, AR, and FOXA1 in mCRPC, and their association with critical nuclear factors and pathways that promote ART resistance.
Article
Chemistry, Physical
Steven J. Kregel, Thomas F. Derrah, Seokjin Moon, David T. Limmer, Gilbert M. Nathanson, Timothy H. Bertram
Summary: The yield of ClNO2 product in competition with hydrolysis of N2O5 in aqueous NaCl solutions only decreases by an average of 4 ± 3% as the temperature changes. This decrease in yield is consistent for NaCl-D2O solutions ranging from 0.0054-0.21 M. Measurements at higher concentrations of NaCl, ranging from 0.54-2.4 M, show similar results.
JOURNAL OF PHYSICAL CHEMISTRY A
(2023)
Article
Oncology
Anthony Williams, Lisa Gutgesell, Larischa de Wet, Phillip Selman, Arunangsu Dey, Mahati Avineni, Isha Kapoor, Megan Mendez, Ryan Brown, Sophia Lamperis, Chuck Blajszczak, Eric Bueter, Steven Kregel, Donald J. Vander Griend, Russell Z. Szmulewitz
Summary: The development of drug resistance in prostate cancer is a challenge, and SOX2 overexpression has been identified as a factor in this resistance. The NR3C1 gene, encoding glucocorticoid receptor, is a target of SOX2 and positively regulates its expression. In addition, SOX2-positive PC cells are insensitive to NHRSI treatment, and the inhibition of WEE1 kinase, along with ARSI or GR modulation, can improve the efficacy of NHRSIs in SOX2-positive PC.
Article
Chemistry, Physical
Steven J. Kregel, Thomas F. Derrah, Seokjin Moon, David T. Limmer, Gilbert M. Nathanson, Timothy H. Bertram
Summary: The temperature dependence of ClNO2 product yield in competition with hydrolysis of N2O5 in aqueous NaCl solutions was measured. The ClNO2 product yield decreased by an average of only 4+/-3% from 5 to 25 degrees C in NaCl-D2O solutions ranging from 0.0054-0.21 M. Measurements at higher NaCl concentrations (0.54-2.4 M) were also within this range. The ratio of the rate constants for chlorination and hydrolysis of N2O5 was determined to be 1150+/-90 at 25 degrees C for NaCl concentrations up to 0.21 M, favoring chlorination. However, this ratio decreased significantly at higher concentrations. An Arrhenius analysis revealed that the activation energy for hydrolysis was only 3.0+/-1.5 kJ/mol larger than for chlorination up to 0.21 M, suggesting similar energetic barriers for Cl- and D2O attack on N2O5 despite their differences in charge and complexity. The preference of N2O5 to undergo chlorination over hydrolysis is attributed to dynamic and entropic factors rather than enthalpic factors, as indicated by the measured preexponential ratio of 300-200+400 favoring chlorination. Molecular dynamics simulations showed distinct solvation between strongly hydrated Cl- and hydrophobically solvated N2O5, suggesting the role of water in mediating interactions between these solvated species and implying diffusion limitations on the chlorination reaction.
JOURNAL OF PHYSICAL CHEMISTRY A
(2023)
Meeting Abstract
Oncology
Lanbo Xiao, Abhijit Parolia, Yuanyuan Qiao, Pushpinder Bawa Pushpinder, Sanjana Eyunni, Rahul Mannan, Sandra E. Carson, Yu Chang, Xiaoju Wang, Yuping Zhang, Josh Vo, Steven Kregel, Stephanie A. Simko, Andrew D. Delekta, Mustapha Jaber, Heng Zheng, Ingrid Apel, Lisa McMurry, Fengyun Su, Rui Wang, Sylvia Wang, Sanjita Sasmal, Leena K. Satyam, Subhendu Mukherjee, Chandrasekhar Abbinen, Kiran Aithal, Mital S. Bhakta, Jay Ghurye, Xuhong Cao, Nora M. Navone, Alexey Nesvizhskii, Rohit Mehra, Ulka Vaishampayan, Marco Blanchette, Yuzhuo Wang, Susanta Samajdar, Murali Ramachandra, Arul M. Chinnaiyan
Meeting Abstract
Oncology
Lanbo Xiao, Abhijit Parolia, Yuanyuan Qiao, Bawa Pushpinder Pushpinder, Sanjana Eyunni, Rahul Mannan, Sandra E. Carson, Yu Chang, Xiaoju Wang, Yuping Zhang, Josh Vo, Steven Kregel, Stephanie A. Simko, Andrew D. Delekta, Mustapha Jaber, Heng Zheng, Ingrid Apel, Lisa McMurry, Fengyun Su, Rui Wang, Sylvia Wang, Sanjita Sasmal, Leena K. Satyam, Subhendu Mukherjee, Chandrasekhar Abbinen, Kiran Aithal, Mital S. Bhakta, Jay Ghurye, Xuhong Cao, Nora M. Navone, Alexey Nesvizhskii, Rohit Mehra, Ulka Vaishampayan, Marco Blanchette, Yuzhuo Wang, Susanta Samajdar, Murali Ramachandra, Arul M. Chinnaiyan
Article
Urology & Nephrology
Daniel C. Moline, Morgan L. Zenner, Alex Burr, Jordan E. Vellky, Larisa Nonn, Donald J. Vander Griend
Summary: Benign prostate hyperplasia and prostate cancer are common diseases characterized by abnormal activation of prostatic tissue. Single-cell RNA sequencing analysis confirmed the presence of a luminal progenitor cell population in the mouse prostate and identified factors involved in prostate organoid regeneration.
AMERICAN JOURNAL OF CLINICAL AND EXPERIMENTAL UROLOGY
(2022)
Article
Multidisciplinary Sciences
Lanbo Xiao, Abhijit Parolia, Yuanyuan Qiao, Pushpinder Bawa, Sanjana Eyunni, Rahul Mannan, Sandra E. Carson, Yu Chang, Xiaoju Wang, Yuping Zhang, Josh N. Vo, Steven Kregel, Stephanie A. Simko, Andrew D. Delekta, Mustapha Jaber, Heng Zheng, Ingrid J. Apel, Lisa McMurry, Fengyun Su, Rui Wang, Sylvia Zelenka-Wang, Sanjita Sasmal, Leena Khare, Subhendu Mukherjee, Chandrasekhar Abbineni, Kiran Aithal, Mital S. Bhakta, Jay Ghurye, Xuhong Cao, Nora M. Navone, Alexey Nesvizhskii, Rohit Mehra, Ulka Vaishampayan, Marco Blanchette, Yuzhuo Wang, Susanta Samajdar, Murali Ramachandra, Arul M. Chinnaiyan
Summary: The SWI/SNF complex plays a crucial role in chromatin remodeling and is altered in over 20% of cancers. A newly developed proteolysis-targeting chimera (PROTAC) named AU-15330 can degrade the SWI/SNF ATPase subunits, SMARCA2 and SMARCA4, leading to inhibition of tumor growth in prostate cancer cells that are sensitive to this degradation. Impeding SWI/SNF-mediated enhancer accessibility could be a promising therapeutic approach for enhancer-addicted cancers.