PMID- 32077199 OWN - NLM STAT- MEDLINE DCOM- 20200422 LR - 20231113 IS - 1349-7006 (Electronic) IS - 1347-9032 (Print) IS - 1347-9032 (Linking) VI - 111 IP - 4 DP - 2020 Apr TI - Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview. PG - 1076-1083 LID - 10.1111/cas.14357 [doi] AB - Rat sarcoma (RAS) is a well-known oncogene that plays important roles in cancer proliferation, cell survival and cell invasion. RAS exists as three major isoforms, Kirsten rat sarcoma (KRAS), Harvey rat sarcoma (HRAS) and neuroblastoma rat sarcoma (NRAS). Mutations of these genes account for approximately 30% of all cancers. Among them, KRAS mutations are the most common, responsible for 85%, followed by NRAS (12%) and HRAS (3%). Although the development of RAS inhibitors has been explored for over the past decade, so far, no effective inhibitor has been found. MicroRNA (miRNA) are a class of small non-coding RNA that control the gene expression of pleural target genes at the post-transcriptional level. MiRNA play critical roles in the physiological and pathological processes at work in cancers, such as cell proliferation, cell death, cell invasion and metastasis. MicroRNA-143 (MIR143) is known to function as a tumor suppressor in a variety of cancers. One of its known mechanisms is suppression of RAS expression and its effector signaling pathways, such as PI3K/AKT and MAPK/ERK. Within the last five years, we developed a potent chemically modified MIR143-3p that enabled us to elucidate the details of the KRAS signaling networks at play in colon and other cancer cells. In this review, we will discuss the role of MIR143-3p in those RAS signaling networks that are related to various biological processes of cancer cells. In addition, we will discuss the possibility of the use of MIR143 as a therapeutic drug for targeting RAS signaling networks. CI - (c) 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. FAU - Tokumaru, Yoshihisa AU - Tokumaru Y AUID- ORCID: 0000-0003-2481-7739 AD - Breast Surgery, Department of Surgical Oncology, Roswell Park Comprehensive Cancer Center, Buffalo, New York. AD - Department of Surgical Oncology, Graduate School of Medicine, Gifu University, Gifu, Japan. FAU - Takabe, Kazuaki AU - Takabe K AUID- ORCID: 0000-0002-6435-4241 AD - Breast Surgery, Department of Surgical Oncology, Roswell Park Comprehensive Cancer Center, Buffalo, New York. AD - Department of Surgery, University at Buffalo Jacobs School of Medicine and Biomedical Sciences, The State University of New York, Buffalo, New York. FAU - Yoshida, Kazuhiro AU - Yoshida K AUID- ORCID: 0000-0003-1408-0104 AD - Department of Surgical Oncology, Graduate School of Medicine, Gifu University, Gifu, Japan. FAU - Akao, Yukihiro AU - Akao Y AUID- ORCID: 0000-0001-8902-5367 AD - United Graduate School of Drug and Medical Information Sciences, Gifu University, Gifu, Japan. LA - eng PT - Journal Article PT - Review DEP - 20200318 PL - England TA - Cancer Sci JT - Cancer science JID - 101168776 RN - 0 (Antineoplastic Agents) RN - 0 (KRAS protein, human) RN - 0 (MIRN143 microRNA, human) RN - 0 (Membrane Proteins) RN - 0 (MicroRNAs) RN - EC 3.6.1.- (GTP Phosphohydrolases) RN - EC 3.6.1.- (NRAS protein, human) RN - EC 3.6.5.2 (HRAS protein, human) RN - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)) SB - IM MH - Antineoplastic Agents/*therapeutic use MH - Cell Proliferation/drug effects MH - GTP Phosphohydrolases/genetics MH - Gene Expression Regulation, Neoplastic/drug effects MH - Humans MH - Membrane Proteins/genetics MH - MicroRNAs/antagonists & inhibitors/*genetics MH - Mutation MH - Oncogenes/*genetics MH - Proto-Oncogene Proteins p21(ras)/genetics MH - Sarcoma/drug therapy/*genetics/pathology MH - Signal Transduction/genetics PMC - PMC7156858 OTO - NOTNLM OT - AKT OT - ERK OT - KRAS positive circuit OT - MAPK OT - MIR143 OT - PI3K OT - RAS COIS- The authors declare no conflict of interest. EDAT- 2020/02/23 06:00 MHDA- 2020/04/23 06:00 PMCR- 2020/04/01 CRDT- 2020/02/21 06:00 PHST- 2019/11/01 00:00 [received] PHST- 2020/02/01 00:00 [revised] PHST- 2020/02/14 00:00 [accepted] PHST- 2020/02/23 06:00 [pubmed] PHST- 2020/04/23 06:00 [medline] PHST- 2020/02/21 06:00 [entrez] PHST- 2020/04/01 00:00 [pmc-release] AID - CAS14357 [pii] AID - 10.1111/cas.14357 [doi] PST - ppublish SO - Cancer Sci. 2020 Apr;111(4):1076-1083. doi: 10.1111/cas.14357. Epub 2020 Mar 18.