Long non-coding RNA: A recently accentuated molecule in chemoresistance in cancer
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Long non-coding RNA: A recently accentuated molecule in chemoresistance in cancer Yang Peng 1,2,3 & Dihong Tang 1 & Meng Zhao 2 & Hiroaki Kajiyama 3 & Fumitaka Kikkawa 3 & Yutaka Kondo 2
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Chemotherapy is one of the important and effective options for cancer treatment in the past decades. Although the response rate of initial chemotherapy is considerably high in certain types of cancers, such as ovarian cancer and lung cancer, the patients frequently suffer from chemoresistance and recurrence of disease. Recent genome-wide studies have shown that the large number of long non-coding RNAs (lncRNAs) are transcribed from the human genome and involved in many biological processes including carcinogenesis. They aberrantly regulate variety of cell functions, such as cell cycle, apoptosis, autophagy, and metabolisms, which are associated with chemosensitivity. Therefore, understanding the biological and clinical impacts of lncRNAs on tumor behavior and its potential as a predictive biomarker for chemotherapy effectiveness is highly desired. In this review, we classify the major mechanisms of lncRNA-related chemoresistance and provide theoretical evidences for targeting lncRNAs in certain types of cancers that may open up new therapeutic paradigm for cancer treatment. Keywords Long non-coding RNA . Epigenetics . Chemoresistance . Cancer
1 Introduction In addition to surgical resection, chemotherapy for cancers reduces residual tumors and prevents their recurrence with increased 5-year survival rate in the past decades [1]. Especially, in the patients with advanced stage of cancer, several studies showed that chemotherapies significantly decreased the mortality rate than surgery or radiation therapy alone [2–4]. Chemotherapy can be classified by their cytotoxic mechanisms as follows: (1) alkylating agents, such as cyclophosphamide (CTX); (2) anti-metabolites that inhibit DNA synthesis, such as fluorouracil (5-FU) and methotrexate
* Yutaka Kondo [email protected] 1
Fourth Department of Gynecologic Oncology, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, 283 Tongzipo Road, Changsha 410000, Hunan, China
2
Division of Cancer Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan
3
Division of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan
(MTX); (3) antibiotics, such as doxorubicin (DOX) and mitomycin C (MMC); (4) DNA topoisomerase inhibitors that prohibit transcription and replication, such as etoposide; (5) mitosis inhibitors, such as paclitaxel (PTX) and vincristine (VCR); and (6) platinum-based drugs that induce DNAplatinum adducts to block DNA repair, such as cisplatin (CDDP) and oxaliplatin (OXA) [5–8]. These chemotherapies exert cytotoxic effects on tumor cells by inducing DNA damage and blocking DNA repair process, thus arresti
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