Experimental and Molecular Medicine

  1226-3613

  2092-6413

  Hàn Quốc

Cơ quản chủ quản:  Korean Society of Med. Biochemistry and Mol. Biology , Springer Nature

Lĩnh vực:
Molecular MedicineMedicine (miscellaneous)Molecular BiologyClinical BiochemistryBiochemistry

Các bài báo tiêu biểu

ROS in cancer therapy: the bright side of the moon
Tập 52 Số 2 - Trang 192-203 - 2020
Bruno Perillo, Marzia Di Donato, Antonio Pezone, Erika Di Zazzo, Pia Giovannelli, Giovanni Galasso, Gabriella Castoria, Antimo Migliaccio
AbstractReactive oxygen species (ROS) constitute a group of highly reactive molecules that have evolved as regulators of important signaling pathways. It is now well accepted that moderate levels of ROS are required for several cellular functions, including gene expression. The production of ROS is elevated in tumor cells as a consequence of increased metabolic rate, gene mutation and relative hypoxia, and excess ROS are quenched by increased antioxidant enzymatic and nonenzymatic pathways in the same cells. Moderate increases of ROS contribute to several pathologic conditions, among which are tumor promotion and progression, as they are involved in different signaling pathways and induce DNA mutation. However, ROS are also able to trigger programmed cell death (PCD). Our review will emphasize the molecular mechanisms useful for the development of therapeutic strategies that are based on modulating ROS levels to treat cancer. Specifically, we will report on the growing data that highlight the role of ROS generated by different metabolic pathways as Trojan horses to eliminate cancer cells.
Mesenchymal stem cells: environmentally responsive therapeutics for regenerative medicine
Tập 45 Số 11 - Trang e54-e54
Matthew B. Murphy, Kathryn Moncivais, Arnold I. Caplan
AbstractMesenchymal stem cells (MSCs) are partially defined by their ability to differentiate into tissues including bone, cartilage and adipose in vitro, but it is their trophic, paracrine and immunomodulatory functions that may have the greatest therapeutic impact in vivo. Unlike pharmaceutical treatments that deliver a single agent at a specific dose, MSCs are site regulated and secrete bioactive factors and signals at variable concentrations in response to local microenvironmental cues. Significant progress has been made in understanding the biochemical and metabolic mechanisms and feedback associated with MSC response. The anti-inflammatory and immunomodulatory capacity of MSC may be paramount in the restoration of localized or systemic conditions for normal healing and tissue regeneration. Allogeneic MSC treatments, categorized as a drug by regulatory agencies, have been widely pursued, but new studies demonstrate the efficacy of autologous MSC therapies, even for individuals affected by a disease state. Safety and regulatory concerns surrounding allogeneic cell preparations make autologous and minimally manipulated cell therapies an attractive option for many regenerative, anti-inflammatory and autoimmune applications.
Writing, erasing and reading histone lysine methylations
Tập 49 Số 4 - Trang e324-e324
Kwangbeom Hyun, Jongcheol Jeon, Kihyun Park, Jaehoon Kim
Regulation and function of AMPK in physiology and diseases
Tập 48 Số 7 - Trang e245-e245
Sang‐Min Jeon
Amino acids in cancer
Tập 52 Số 1 - Trang 15-30 - 2020
Elizabeth L. Lieu, Tu Nguyen, Shawn Rhyne, Jiyeon Kim
AbstractOver 90 years ago, Otto Warburg’s seminal discovery of aerobic glycolysis established metabolic reprogramming as one of the first distinguishing characteristics of cancer1. The field of cancer metabolism subsequently revealed additional metabolic alterations in cancer by focusing on central carbon metabolism, including the citric acid cycle and pentose phosphate pathway. Recent reports have, however, uncovered substantial non-carbon metabolism contributions to cancer cell viability and growth. Amino acids, nutrients vital to the survival of all cell types, experience reprogrammed metabolism in cancer. This review outlines the diverse roles of amino acids within the tumor and in the tumor microenvironment. Beyond their role in biosynthesis, they serve as energy sources and help maintain redox balance. In addition, amino acid derivatives contribute to epigenetic regulation and immune responses linked to tumorigenesis and metastasis. Furthermore, in discussing the transporters and transaminases that mediate amino acid uptake and synthesis, we identify potential metabolic liabilities as targets for therapeutic intervention.
Intracellular sensing of viral genomes and viral evasion
Tập 51 Số 12 - Trang 1-13 - 2019
Hyun‐Cheol Lee, Kiramage Chathuranga, Jong‐Soo Lee
AbstractDuring viral infection, virus-derived cytosolic nucleic acids are recognized by host intracellular specific sensors. The efficacy of this recognition system is crucial for triggering innate host defenses, which then stimulate more specific adaptive immune responses against the virus. Recent studies show that signal transduction pathways activated by sensing proteins are positively or negatively regulated by many modulators to maintain host immune homeostasis. However, viruses have evolved several strategies to counteract/evade host immune reactions. These systems involve viral proteins that interact with host sensor proteins and prevent them from detecting the viral genome or from initiating immune signaling. In this review, we discuss key regulators of cytosolic sensor proteins and viral proteins based on experimental evidence.
Combination of anti-angiogenic therapy and immune checkpoint blockade normalizes vascular-immune crosstalk to potentiate cancer immunity
Tập 52 Số 9 - Trang 1475-1485 - 2020
Won Suk Lee, Hannah Yang, Hong Jae Chon, Chan Kim
AbstractCancer immunotherapy with immune checkpoint inhibitors (ICIs) has revolutionized the treatment of advanced cancers. However, the tumor microenvironment (TME) functions as a formidable barrier that severely impairs the efficacy of ICIs. While the crosstalk between tumor vessels and immune cells determines the nature of anti-tumor immunity, it is skewed toward a destructive cycle in growing tumors. First, the disorganized tumor vessels hinder CD8+T cell trafficking into the TME, disable effector functions, and even kill T cells. Moreover, VEGF, the key driver of angiogenesis, interferes with the maturation of dendritic cells, thereby suppressing T cell priming, and VEGF also induces TOX-mediated exhaustion of CD8+T cells. Meanwhile, a variety of innate and adaptive immune cells contribute to the malformation of tumor vessels. Protumoral M2-like macrophages as well as TH2 and Treg cells secrete pro-angiogenic factors that accelerate uncontrolled angiogenesis and promote vascular immaturity. While CD8+T and CD4+TH1 cells suppress angiogenesis and induce vascular maturation by secreting IFN-γ, they are unable to infiltrate the TME due to malformed tumor vessels. These findings led to preclinical studies that demonstrated that simultaneous targeting of tumor vessels and immunity is a viable strategy to normalize aberrant vascular-immune crosstalk and potentiate cancer immunotherapy. Furthermore, this combination strategy has been evidently demonstrated through recent pivotal clinical trials, granted approval from FDA, and is now being used in patients with kidney, liver, lung, or uterine cancer. Overall, combining anti-angiogenic therapy and ICI is a valid therapeutic strategy that can enhance cancer immunity and will further expand the landscape of cancer treatment.
Exosomes from adipose-derived stem cells overexpressing Nrf2 accelerate cutaneous wound healing by promoting vascularization in a diabetic foot ulcer rat model
Tập 50 Số 4 - Trang 1-14 - 2018
Xue Li, Xiaoyun Xie, Weishuai Lian, Rongfeng Shi, Shengnan Han, Haijun Zhang, Ligong Lu, Maoquan Li
Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex
Tập 52 Số 2 - Trang 183-191 - 2020
Youn‐Sang Jung, Jae‐Il Park
AbstractWnt/β-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt/β-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. In this review, we discuss the Wnt inhibitors currently being used in clinical trials and suggest how additional cancer-specific regulators could be utilized to treat Wnt signaling-associated cancer.