Article
Oncology
Shuai Huang, Xudong Zhang, Kai Luo, Li Jiang, Jianhua Jiang, Renfeng Li
Summary: In this study, OSBP2 was found to be highly expressed in PDAC and its upregulation promoted the progression of PDAC, including increased cell migration, invasion, proliferation, chemotherapy resistance, and decreased apoptosis. Furthermore, overexpression of OSBP2 resulted in downregulation of the cell adhesion molecule E-cadherin and upregulation of other transcription factors. Therefore, OSBP2 may serve as a potential diagnostic and therapeutic target for PDAC.
FRONTIERS IN ONCOLOGY
(2022)
Review
Medicine, General & Internal
Wiktoria Maria Izdebska, Jaroslaw Daniluk, Jacek Niklinski
Summary: Pancreatic ductal adenocarcinoma (PDAC) is a common and fatal neoplasm in humans. Current research focuses on two fields: non-coding RNA (especially microRNA and long non-coding RNA) and the microbiota. Recent findings show that miRNA can affect specific bacteria in the gut microbiome that contribute to pancreatic carcinogenesis, and the microbiome can also impact miRNA expression. Combining the microbiome and non-coding RNA may offer potential strategies for suppressing PDAC development, but more research is needed to fully understand and utilize these approaches for diagnosis, treatment, and prevention.
JOURNAL OF CLINICAL MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Ching-Chung Ko, Yao-Yu Hsieh, Pei-Ming Yang
Summary: Epithelial-to-mesenchymal transition (EMT) is a biological process that promotes cancer cell dissemination and drug resistance. This study revealed that overexpression of MIR31HG in pancreatic ductal adenocarcinoma (PDAC) patients is associated with poorer disease-free survival, as well as upregulation of genes related to TGF beta signaling and EMT. In vitro experiments further demonstrated that TGF beta induces MIR31HG expression and knockdown of MIR31HG reverses TGF beta-induced EMT phenotypes and cancer cell migration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Oncology
Maria Mortoglou, Zoey Kathleen Tabin, E. Damla Arisan, Hemant M. Kocher, Pinar Uysal-Onganer
Summary: PDAC is an aggressive malignancy with poor survival rates and challenging early detection. Current standard of care involves multimodality treatment, with the common diagnostic biomarker CA 19-9 showing limitations in specificity. Non-coding RNAs play a role in PDAC and their functions in diagnosis and treatment are under discussion.
TRANSLATIONAL ONCOLOGY
(2021)
Article
Oncology
Xing Huang, Feng Zhao, Quan Wu, Zitong Wang, Haiyue Ren, Qiqi Zhang, Zhe Wang, Jin Xu
Summary: For patients with pancreatic cancer, KIF2C is abnormally expressed and affects the prognosis. KIF2C promotes the proliferation, invasion, and metastasis of pancreatic cancer. The overexpression of KIF2C has potential therapeutic implications for pancreatic ductal adenocarcinoma (PDAC).
Article
Biochemistry & Molecular Biology
Maria Mortoglou, Francesc Miralles, Elif Damla Arisan, Alwyn Dart, Stipo Jurcevic, Sigrun Lange, Pinar Uysal-Onganer
Summary: This study investigated the role of miR-21 in cancer stem cells (CSCs) and its association with the aggressiveness of PDAC. Knockout of miR-21 resulted in reversed expressions of CSC markers and suppressed cellular invasion and proliferation. These findings suggest that miR-21 is involved in the stemness of PDAC cells, may play roles in mesenchymal transition, and serves as a novel functional biomarker for PDAC aggressiveness.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Tugba Mehmetoglu-Gurbuz, Rajkumar Lakshmanaswamy, Karla Perez, Mayra Sandoval, Casandra A. Jimenez, Jackelyn Rocha, Rachel Madeline Goldfarb, Courtney Perry, Alejandra Bencomo, Nishkala Neela, Jose A. Barragan, Raquel Sanchez, Risa Mia Swain, Ramadevi Subramani
Summary: This study found that nimbolide (NB) effectively blocks the growth and metastasis of pancreatic ductal adenocarcinomas (PDACs) by suppressing the expression and activity of superoxide dismutase 2 (SOD2). NB induces high levels of reactive oxygen species (ROS) generation, leading to increased apoptosis and reduced progression of PDACs. SOD2 plays an important role in regulating NB-induced ROS generation, presenting itself as a therapeutic option for PDACs.
Review
Biochemistry & Molecular Biology
Shailendra K. Gautam, Surinder K. Batra, Maneesh Jain
Summary: Immunosuppression is a major factor contributing to the poor survival of patients with metastatic pancreatic ductal adenocarcinoma (PDAC). Although immunotherapies have shown promise in certain cancers, limited responses have been achieved in PDAC due to specific mechanisms that regulate the poor response to immunotherapy. The immunosuppressive microenvironment, driven by oncogenic mutations, tumor secretome, non-coding RNAs, and tumor microbiome, plays a role in local growth and distant metastasis of PDAC. Metastatic immune microenvironment differs from primary tumors in stromal and immune cell composition, functionality, and metabolism, confounding the immunotherapy response in metastatic PDAC.
Article
Multidisciplinary Sciences
Mengyuan Xu, Lei Fang, Xin Guo, Henan Qin, Rui Sun, Zhen Ning, Aman Wang
Summary: The study revealed that RIOK3 promotes invasion and metastasis of pancreatic ductal adenocarcinoma (PDAC) by modulating focal adhesion kinase (FAK) protein expression and phosphorylation, providing a potential new therapeutic target for PDAC treatment. Additionally, RIOK3-related genes were found to be upregulated in PDAC patients and associated with poor prognosis.
Article
Oncology
Marie-Lucie Racu, Laetitia Lebrun, Andrea Alex Schiavo, Claude Van Campenhout, Sarah De Clercq, Lara Absil, Esmeralda Minguijon Perez, Calliope Maris, Christine Decaestecker, Isabelle Salmon, Nicky D'Haene
Summary: Pancreatic ductal adenocarcinoma (PDAC) has a low survival rate and its incidence is increasing over time. Understanding the molecular mechanisms behind metastasis and chemoresistance in PDAC is crucial, as these are the main causes of death in patients. SMAD4 is deactivated in half of PDAC cases and its loss is associated with worse overall survival and metastasis. SMAD4 is a key transducer in the TGF-beta pathway, which plays a role in epithelial-mesenchymal transition (EMT). EMT is a biological process where epithelial cells lose their characteristics and acquire a more mesenchymal phenotype, leading to increased motility. Recent studies suggest that cells may undergo intermediate states during EMT, known as epithelial-mesenchymal plasticity (EMP), which exhibit enhanced aggressiveness and more efficient metastasis. This review aims to summarize and analyze current knowledge on SMAD4 loss in PDAC patients and investigate its potential role in EMP, in order to better understand its function in PDAC carcinogenesis.
Article
Biochemistry & Molecular Biology
Yanfen Lian, Dongxiao Jiang, Jiangtao Sun
Summary: The study found that miR-33a-5p expression is significantly decreased in PDAC tissues and cell lines, and its downregulation is significantly associated with TNM staging and lymph node metastasis. Overexpression of miR-33a-5p inhibits cell proliferation, migration, and invasion in SW1990 and PANC-1 cells, while knockdown of miR-33a-5p promotes these processes in BxPC-3 and ASPC-1 cells. Additionally, RAP2A was identified as a direct target of miR-33a-5p in PDAC cells, and its overexpression reversed the suppressive effects of miR-33a-5p in SW1990 and PANC-1 cells.
CELLULAR & MOLECULAR BIOLOGY LETTERS
(2021)
Review
Biochemistry & Molecular Biology
Roman Bubin, Romans Uljanovs, Ilze Strumfa
Summary: The discovery of cancer stem cells (CSCs) in leukemia has led to active research on stemness in neoplastic tissues. CSCs are a subpopulation of malignant cells with unique properties, including a dedifferentiated state, self-renewal, pluripotency, resistance to therapy, epigenetic alterations, and higher tumorigenicity. CSCs have been confirmed in various malignancies, including pancreatic ductal adenocarcinoma, which has a poor prognosis. This review aims to summarize the current knowledge on the markers and molecular features of CSCs in pancreatic ductal adenocarcinoma and the therapeutic options for their elimination.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Oncology
Kostas Palamaris, Evangelos Felekouras, Stratigoula Sakellariou
Summary: Pancreatic ductal adenocarcinoma (PDAC) is a deadly malignancy characterized by aggressive behavior and resistance to chemotherapy, with emerging evidence pointing to epithelial to mesenchymal transition (EMT) as a key driver of disease progression and drug resistance. EMT allows cancer cells to transition to a more mesenchymal state, contributing to tumor dissemination and chemoresistance in PDAC.
Article
Biochemistry & Molecular Biology
Hendrik Ungefroren, Ruediger Braun, Olha Lapshyna, Bjoern Konukiewitz, Ulrich F. Wellner, Hendrik Lehnert, Jens-Uwe Marquardt
Summary: This study reveals the inhibitory role of ALK2 in cell migration in pancreatic ductal adenocarcinoma (PDAC) cells, which is mediated by transforming growth factor beta 1 (TGF beta 1). ALK2 suppresses the expression of RAC1/RAC1b proteins and acts together with RAC1b in a self-perpetuating negative feedback loop. The antimigratory function of ALK2 is particularly crucial in protecting epithelial subtype PDAC cells from invasion.
Review
Cell Biology
Tianyi Zhang, Yanxian Ren, Pengfei Yang, Jufang Wang, Heng Zhou
Summary: Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer with a high deposition of extracellular matrix (ECM) and poor prognosis. ECM proteins derived from tumor cells reduce the effectiveness of conventional cancer treatment and contribute to tumor progression and metastasis. Cancer-associated fibroblasts (CAFs) in the ECM are promising targets for novel anti-tumor interventions.
CELL DEATH & DISEASE
(2022)
Meeting Abstract
Gastroenterology & Hepatology
Keisuke Yamakita, Yohei Kitano, Kenji Takahashi, Hidetaka Iwamoto, Yuko Suzuki, Kazunobu Aso, Mitsuyoshi Okada, Yosui Tamaki, Yu Ota, Shin Otake, Masakazu Haneda
GASTROINTESTINAL ENDOSCOPY
(2016)
Article
Oncology
Kenji Takahashi, Yu Ota, Takayuki Kogure, Yuko Suzuki, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Satoshi Fujii, Masakazu Haneda, Tushar Patel, Tsuguhito Ota
Review
Gastroenterology & Hepatology
Julia Driscoll, Cody Wehrkamp, Yu Ota, Jonathan N. Thomas, Irene K. Yan, Tushar Patel
Summary: Extracellular vesicles (EVs) are biological nano-sized vesicles released from cells that have potential therapeutic applications in liver diseases. They can be used directly as therapeutics or modified for the delivery of therapeutic cargo, showing promise in treating chronic and acute liver diseases. EV-based therapeutics offer a viable approach to target hepatic pathophysiology.
Article
Biochemistry & Molecular Biology
Yu Ota, Kenji Takahashi, Shin Otake, Yosui Tamaki, Mitsuyoshi Okada, Irene Yan, Kazunobu Aso, Satoshi Fujii, Tushar Patel, Masakazu Haneda
Summary: Extracellular vesicles within the cellular secretome play a crucial role in tumor growth, with normal cells transferring miR-195 to cholangiocarcinoma cells via EVs to modulate their growth and behavior. The findings highlight the significance of EV-mediated transfer of miRNA as a mechanism in tumor development, providing potential therapeutic opportunities for targeting human cholangiocarcinoma.
Meeting Abstract
Gastroenterology & Hepatology
K. Koyama, K. Takahashi, Y. Ota, Y. Suzuki, H. Iwamoto, K. Yamakita, Y. Kitano, T. Ota
Meeting Abstract
Gastroenterology & Hepatology
Kenji Takahashi, Yu Ota, Yuko Suzuki, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Tsuguhito Ota
Meeting Abstract
Gastroenterology & Hepatology
Kenji Takahashi, Yu Ota, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Yuichi Makino, Tsuguhito Ota
Meeting Abstract
Gastroenterology & Hepatology
Yu Ota, Kenji Takahashi, Shin Otake, Yosui Tamaki, Mitsuyoshi Okada, Kazunobu Aso, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Tsuguhito Ota
Meeting Abstract
Gastroenterology & Hepatology
K. Takahashi, Y. Ota, H. Iwamoto, K. Yamakita, Y. Kitano, Y. Makino
Meeting Abstract
Gastroenterology & Hepatology
Yu Ota, Kenji Takahashi, Shin Otake, Yosui Tamaki, Mitsuyoshi Okada, Kazunobu Aso, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Yuichi Makino
Meeting Abstract
Gastroenterology & Hepatology
Yu Ota, Kenji Takahashi, Shin Otake, Yosui Tamaki, Mitsuyoshi Okada, Kazunobu Aso, Yuko Suzuki, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Yuichi Makino
Meeting Abstract
Gastroenterology & Hepatology
Y. Suzuki, K. Takahashi, H. Iwamoto, K. Yamakita, Y. Kitano, Y. Ota, Y. Tamaki, M. Okada, K. Aso, M. Haneda
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
(2015)
Meeting Abstract
Gastroenterology & Hepatology
Kenji Takahashi, Yu Ota, Yuko Suzuki, Hidetaka Iwamoto, Keisuke Yamakita, Yohei Kitano, Ryuji Sudo, Yosui Tamaki, Mitsuyoshi Okada, Kazunobu Aso, Yuichi Makino, Masakazu Haneda
Meeting Abstract
Gastroenterology & Hepatology
Keisuke Yamakita, Yohei Kitano, Ai Takasoe, Yuko Suzuki, Hidetaka Iwamoto, Masako Imazawa, Kenji Takahashi, Kaori Wada, Yu Ota, Ryuji Sudou, Yosui Tamaki, Mitsuyoshi Okada, Kazunobu Aso, Masakatsu Haneda
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
(2014)