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Cancer letters 20건

  1. [해외논문]   Editorial Board   SCI SCIE


    Cancer letters v.415 ,pp. ii - ii , 2018 , 0304-3835 ,

    초록

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  2. [해외논문]   Oncogenic Kit signalling on the Golgi is suppressed by blocking secretory trafficking with M-COPA in gastrointestinal stromal tumours   SCI SCIE

    Obata, Yuuki (Division of Immunobiology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda 278-0022, Chiba, Japan ) , Horikawa, Keita (Division of Immunobiology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda 278-0022, Chiba, Japan ) , Shiina, Isamu (Department of Applied Chemistry, Faculty of Science, Tokyo University of Science, Shinjuku-ku 162-8601, Tokyo, Japan ) , Takahashi, Tsuyoshi (Department of Surgery, Graduate School of Medicine, Osaka University, Suita 565-0871, Osaka, Japan ) , Murata, Takatsugu (Department of Applied Chemistry, Faculty of Science, Tokyo University of Science, Shinjuku-ku 162-8601, Tokyo, Japan ) , Tasaki, Yasutaka (Department of Applied Chemistry, Faculty of Science, Tokyo University of Science, Shinjuku-ku 162-8601, Tokyo, Japan ) , Suzuki, Kyohei (Department of Applied Chemistry, Faculty of Science, Tokyo University of Science, Shinjuku-ku 162-8601, Tokyo, Japan ) , Yonekura, Keita (Department of Applied Chemistry, Faculty of Science, Tokyo University of Science, Shinjuku-ku 162-8601, Tokyo, Japan ) , Esumi, Hiroyasu (Division of Clinical Research, Research Inst) , Nishida, Toshirou , Abe, Ryo
    Cancer letters v.415 ,pp. 1 - 10 , 2018 , 0304-3835 ,

    초록

    Abstract Most gastrointestinal stromal tumours (GISTs) are caused by constitutively active mutations in Kit tyrosine kinase. The drug imatinib, a specific Kit inhibitor, improves the prognosis of metastatic GIST patients, but these patients become resistant to the drug by acquiring secondary mutations in the Kit kinase domain. We recently reported that a Kit mutant causes oncogenic signals only on the Golgi apparatus in GISTs. In this study, we show that in GIST, 2- m ethyl co pro p hilin a mide (M-COPA, also known as “AMF-26”), an inhibitor of biosynthetic protein trafficking from the endoplasmic reticulum (ER) to the Golgi, suppresses Kit autophosphorylation at Y703/Y721/Y730/Y936, resulting in blockade of oncogenic signalling. Results of our M-COPA treatment assay show that Kit Y703/Y730/Y936 in the ER are dephosphorylated by protein tyrosine phosphatases (PTPs), thus the ER-retained Kit is unable to activate downstream molecules. ER-localized Kit Y721 is not phosphorylated, but not due to PTPs. Importantly, M-COPA can inhibit the activation of the Kit kinase domain mutant, resulting in suppression of imatinib-resistant GIST proliferation. Our study demonstrates that Kit autophosphorylation is spatio-temporally regulated and may offer a new strategy for treating imatinib-resistant GISTs. Highlights Autophosphorylation of Kit mutant at Y703/Y730/Y721/Y936 occurs mainly on the Golgi in GISTs. M-COPA blocks Kit trafficking from the ER to the Golgi, leading to suppression of oncogenic signals. Kit Y703/Y730/Y936 in the ER are dephosphorylated by protein tyrosine phosphatases. M-COPA inhibits oncogenic signalling by targeting drug-resistant Kit mutant.

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  3. [해외논문]   HBXIP-elevated methyltransferase METTL3 promotes the progression of breast cancer via inhibiting tumor suppressor let-7g   SCI SCIE

    Cai, Xiaoli (State Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Wang, Xiao (State Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Cao, Can (State Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Gao, Yuen (State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Zhang, Shuqin (State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Yang, Zhe (State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China ) , Liu, Yunxia (State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Lif) , Zhang, Xiaodong , Zhang, Weiying , Ye, Lihong
    Cancer letters v.415 ,pp. 11 - 19 , 2018 , 0304-3835 ,

    초록

    Abstract Methyltransferase-like 3 (METTL3) is involved in RNA metabolism through N6-methyladenosine (m 6 A) modification. However, whether METTL3 participates in the progression of breast cancer is unclear. Aberrant expression of Mammalian hepatitis B X-interacting protein (HBXIP) drives the aggressiveness of breast cancer. Here, we are interested in the potential links between HBXIP and METTL3 in breast cancer. We showed that the expression of METTL3 was positively related to that of HBXIP in clinical breast cancer tissues. Moreover, HBXIP could up-regulate METTL3 in breast cancer cells. Mechanistically, HBXIP modulated METTL3 by inhibiting miRNA let-7g, which down-regulated the expression of METTL3 by targeting its 3′UTR. Strikingly, we found that METTL3 promoted the expression of HBXIP through m 6 A modification. Furthermore, overexpressed HBXIP could rescue the inhibited-proliferation and enhanced-apoptosis induced by silencing of METTL3 in breast cancer cells. Thus, we conclude that HBXIP up-regulates METTL3 by suppressing let-7g, in which METTL3 increased HBXIP expression forming a positive feedback loop of HBXIP/let-7g/METTL3/HBXIP, leading to accelerated cell proliferation in breast cancer. Our finding provides new insights into the mechanism of the mutual regulation between HBXIP and METTL3 in the progression of breast cancer. Highlights The expression levels of METTL3 are high in clinical breast cancer samples. METTL3 is up-regulated by the oncoprotein HBXIP in breast cancer cells. HBXIP modulates the expression of METTL3 by inhibiting the tumor suppressor let-7g. METTL3 enhances the expression of HBXIP through m 6 A modification. HBXIP-elevated METTL3 promotes the malignant growth of breast cancer.

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  4. [해외논문]   Dicer reprograms stromal fibroblasts to a pro-inflammatory and tumor-promoting phenotype in ovarian cancer   SCI SCIE

    Yang, Zongyuan (Corresponding author.) , Jin, Ping , Xu, Sen , Zhang, Taoran , Yang, Xin , Li, Xiaoting , Wei, Xiao , Sun, Chaoyang , Chen, Gang , Ma, Ding , Gao, Qinglei
    Cancer letters v.415 ,pp. 20 - 29 , 2018 , 0304-3835 ,

    초록

    Abstract Inflammation and host stromal activation contribute significantly to ovarian cancer (OC) initiation and malignant progression. However, the complex reciprocal interactions between them are largely unknown. Here, we discovered that the tumor suppressor gene Dicer was paradoxically overexpressed in ovarian tumor stroma, and induced fibroblast activation and stromal inflammation. Dicer transformed normal fibroblasts to a carcinoma-associated fibroblast (CAF)-like state, which was morphologically spread out and functionally activated to fuel tumor invasion and metastasis. Attenuation of Dicer hampered CAF characteristics, diminished stromal inflammation and the role of fibroblasts in supporting tumor growth. Moreover, Dicer drove the expression of an “inflammatory signature” in fibroblasts that could be used to discriminate normal and cancerous stroma and predict the survival of patients with OC. Finally, the nuclear factor κ B (NFκB) signaling was demonstrated to be responsible for Dicer effect on fibroblast activation and stromal inflammation, through microRNA (miR)-6780b. Our study represents the first report that characterizes Dicer expression and function in the tumor stroma, and highlights its pro-metastatic role in this context. Additionally, we suggest that the Dicer-miR6780b-NFκB cascade is an attractive target of choice in stroma-oriented OC therapy. Highlights Dicer was specifically overexpressed in ovarian tumor stroma. Dicer plays a pro-metastatic role in ovarian tumor stroma. Dicer drove an inflammatory signature in stromal fibroblasts. Dicer regulates fibroblast activation and stromal inflammation through NFκB signaling. Dicer downregulates mir6780b, which attenuates the NFκB pathways in fibroblasts.

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  5. [해외논문]   IMP2 and IMP3 cooperate to promote the metastasis of triple-negative breast cancer through destabilization of progesterone receptor   SCI SCIE

    Kim, Hye-Youn (Corresponding author. Laboratory of Cancer Cell Biology, Department of Biochemistry, School of Medicine, Gachon University, 155 Gaetbel-ro Yeonsu-gu, Incheon, 21999, Republic of Korea.) , Ha Thi, Huyen Trang , Hong, Suntaek
    Cancer letters v.415 ,pp. 30 - 39 , 2018 , 0304-3835 ,

    초록

    Abstract Triple-negative breast cancer (TNBC) is one of the most aggressive malignancies and is associated with high mortality rates due to the lack of effective therapeutic targets. In this study, we demonstrated that insulin-like growth factor-II mRNA-binding protein 2 and 3 (IMP2 and IMP3) are specifically overexpressed in TNBC and cooperate to promote cell migration and invasion. Downregulation of both IMP2 and IMP3 in TNBC cells was found to produce a synergistic effect in suppressing cell invasion and invadopodia formation, whereas overexpression of IMP2 and IMP3 in luminal subtype cells enhanced epithelial-mesenchymal transition and metastasis. We also showed that IMP2 and IMP3 are direct targets of microRNA-200a (miR-200a), which is downregulated in TNBC. Conversely, IMP2 and IMP3 suppressed the transcription of miR-200a by destabilizing progesterone receptor (PR) mRNA through recruitment of the CCR4-NOT transcription complex subunit 1 (CNOT1) complex. Together, our findings suggest that IMP2 and IMP3 partially determine the characteristic phenotype and synergistically promote the metastasis of TNBC by downregulating PR. The identified IMP2/3-miR-200a-PR axis represents a novel double-negative feedback loop and serves as a new potential therapeutic target for the treatment of TNBC. Highlights IMP2 and IMP3 synergistically promote the migration and metastasis of TNBC. miR-200a directly regulates the expression of IMP2 and IMP3. IMP2 and IMP3 negatively regulate the expression of miR-200a at transcriptional level. IMP2 and IMP3 reduce the stability of PR mRNA by recruiting the CNOT1 complex. IMP2/3-miR-200a-PR axis can be a novel therapeutic target against metastasis of TNBC.

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  6. [해외논문]   Interplay between the lung microbiome and lung cancer   SCI SCIE

    Mao, Qixing (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, 210009, PR China ) , Jiang, Feng (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, 210009, PR China ) , Yin, Rong (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, 210009, PR China ) , Wang, Jie (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, 210009, PR China ) , Xia, Wenjie (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, 210009, PR China ) , Dong, Gaochao (Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical) , Ma, Weidong , Yang, Yao , Xu, Lin , Hu, Jianzhong
    Cancer letters v.415 ,pp. 40 - 48 , 2018 , 0304-3835 ,

    초록

    Abstract The human microbiome confers benefits or disease susceptibility to the human body through multiple pathways. Disruption of the symbiotic balance of the human microbiome is commonly found in systematic diseases such as diabetes, obesity, and chronic gastric diseases. Emerging evidence has suggested that dysbiosis of the microbiota may also play vital roles in carcinogenesis at multiple levels, e.g., by affecting metabolic, inflammatory, or immune pathways. Although the impact of the gut microbiome on the digestive cancer has been widely explored, few studies have investigated the interplay between the microbiome and lung cancer. Some recent studies have shown that certain microbes and microbiota dysbiosis are correlated with development of lung cancer. In this mini-review, we briefly summarize current research findings describing the relationship between the lung microbiome and lung cancer. We further discuss the potential mechanisms through which the lung microbiome may play a role in lung carcinogenesis and impact lung cancer treatment. A better knowledge of the interplay between the lung microbiome and lung cancer may promote the development of innovative strategies for early prevention and personalized treatment in lung cancer. Highlights The Lungs are not sterile, and the lung microbiome is associated with lung health. The lung microbiome is linked to lung cancer. Microbial dysbiosis may modulate the risk of malignancy at multiple levels.

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  7. [해외논문]   LncRNAs and CircRNAs from the same gene: Masterpieces of RNA splicing   SCI SCIE

    Huang, Ma-Sha (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Zhu, Tao (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Li, Ling (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Xie, Pan (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Li, Xi (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Zhou, Hong-Hao (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China ) , Liu, Zhao-Qian (Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China)
    Cancer letters v.415 ,pp. 49 - 57 , 2018 , 0304-3835 ,

    초록

    Abstract Accumulating evidence has shown that lncRNAs and circRNAs are novel regulators of gene expression. The discovery of numerous lncRNAs and circRNAs, and investigation into their structures and functions will contribute to our understanding of the pathogenesis of diseases as well as better prevention, diagnosis, and treatment of diseases. There is a close relationship between circRNAs and lncRNAs regarding their origins and functions. Recent studies have shown that non-coding linear and circular transcripts can be transcribed from the same gene and are potential super-enhancers modulating gene transcription. In this review, we summarize the categories, characteristics, biological functions and databases of both lncRNAs and circRNAs, focusing on their transcriptions derived from the same gene, which might give us a deeper understanding of and enable us to better recognize and distinguish their physiological roles. Highlights We screened lncRNAs and circRNAs transcripts derived from 8 genes. We summarized the functions of lncRNAs and circRNAs from the same gene. We compared categories, characteristics, biological functions and databases of lncRNAs and circRNAs.

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  8. [해외논문]   NFYB-induced high expression of E2F1 contributes to oxaliplatin resistance in colorectal cancer via the enhancement of CHK1 signaling   SCI SCIE

    Fang, Zejun (Central Laboratory, Sanmen People's Hospital of Zhejiang, Sanmenwan Branch of the First Affiliated Hospital, Zhejiang University, Sanmen, 317100, China ) , Gong, Chaoju (Xuzhou Key Laboratory of Ophthalmology, The First People's Hospital of Xuzhou, Xuzhou, 221002, China ) , Yu, Songshan (Central Laboratory, Sanmen People's Hospital of Zhejiang, Sanmenwan Branch of the First Affiliated Hospital, Zhejiang University, Sanmen, 317100, China ) , Zhou, Weihua (Central Laboratory, Sanmen People's Hospital of Zhejiang, Sanmenwan Branch of the First Affiliated Hospital, Zhejiang University, Sanmen, 317100, China ) , Hassan, Waseem (Department of Pharmacy, The Islamia University of Bahawalpur, Bahawalpur, 60000, Pakistan ) , Li, Hongzhang (Department of Gastroenterology, Sanmen People's Hospital of Zhejiang, Sanmen, 317100, China ) , Wang, Xue (Department of Pharmacology, China Pharmaceutical University, Nanjing, 210009, China ) , Hu, Yanyan (Central Laboratory, Sanmen People's Hospital of Zhejiang, Sanmenwan Branch of the First Affiliated Hospital, Zhejiang University, Sanmen, 317100, China ) , Gu, Kaipeng (Central L) , Chen, Xixi , Hong, Bing , Bao, Yuyan , Chen, Xiang , Zhang, Xiaomin , Liu, Hong
    Cancer letters v.415 ,pp. 58 - 72 , 2018 , 0304-3835 ,

    초록

    Abstract As a third-generation platinum drug, oxaliplatin has been widely applied in colorectal cancer (CRC); however, acquired resistance to oxaliplatin has become a major obstacle. In the present study, we found that the nuclear transcription factor Y subunit beta (NFYB) and E2F transcription factor 1 (E2F1) expression levels were significantly higher in oxaliplatin-resistant DLD1 and RKO CRC (OR-CRC) cells than in non-resistant cells. Additionally, highly expressed NFYB transactivated the E2F1 gene, which is important to maintain oxaliplatin resistance in OR-CRC cells. And Sirt1-dependent deacetylation suppresses the proapoptotic activity of E2F1 in OR-CRC cells. Through profiling the transcriptome of OR-CRC cells following E2F1 knockdown, CHK1 was identified as a target of E2F1. Deprivation of CHK1 sensitized OR-CRC cells to oxaliplatin. In vitro and in vivo phenotype experiments confirmed that an intact NFYB-E2F1-CHK1 axis was required to suppress oxaliplatin-induced apoptosis and maintain the tumorigenicity in OR-CRC cells. Knockdown of E2F1 in OR-CRC cells also decreased the expression of Pol κ, which was essential for CHK1 activation. Consistently, a high level of NFYB, E2F1, or CHK1 predicted poor survival in CRC patients, especially with oxaliplatin treatment. Collectively, the NFYB-E2F1 pathway displays a crucial role in the chemoresistance of OR-CRC by inducing the expression and activation of CHK1, providing a possible therapeutic target for oxaliplatin resistance in CRC. Highlights Overactivation of NFYB-E2F1-CHK1 in OR-CRC cells confers oxaliplatin-resistance. Highly expressed E2F1 increases Pol κ level and CHK1 activation in OR-CRC cells. Deacetylation of E2F1 by Sirt1 inhibits E2F1-induced apoptosis in OR-CRC cells. High level of NFYB, E2F1, or CHK1 indicates a poor survival in CRC patients.

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  9. [해외논문]   Ginsenoside Rg3 sensitizes hypoxic lung cancer cells to cisplatin via blocking of NF-κB mediated epithelial–mesenchymal transition and stemness   SCI SCIE

    Wang, Jingjing (Department of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, PR China ) , Tian, Lili (Department of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, PR China ) , Khan, Muhammad Noman (Department of Biochemistry and Molecular Biology, Liaoning Provincial Core Lab of Glycobiology and Glycoengineering, Dalian Medical University, Dalian 116044, PR China ) , Zhang, Li (Department of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, PR China ) , Chen, Qun (Department of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, PR China ) , Zhao, Yi (Department of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, PR China ) , Yan, Qiu (Department of Biochemistry and Molecular Biology, Liaoning Provincial Core Lab of Glycobiology and Glycoengineering, Dalian Medical University, Dalian 116044, PR China ) , Fu, Li (Engineering Technology Center of Traditional Chinese Medicine, Dalian 116600, PR China ) , Liu, Jiwei (Department of Oncology, First Affiliated)
    Cancer letters v.415 ,pp. 73 - 85 , 2018 , 0304-3835 ,

    초록

    Abstract Cisplatin is a first line chemotherapy in lung cancer, but decreased susceptibility may limit its application. In solid tumors, hypoxia alters the microenvironment and is associated with proliferation, metastasis, and drug sensitivity. The hypoxia-induced desensitization of cisplatin is not clearly elucidated. 20 (R)-Ginsenoside (Rg3), the traditional Chinese medicine, is extracted from ginseng and has antitumor activities. In this study, we evaluated if Rg3 is effective in improving cisplatin sensitivity by blocking hypoxia. We found that the inhibition of proliferation potential by cisplatin was reduced in cobalt chloride (CoCl 2 )-induced hypoxia in lung cancer cells. Hypoxia caused alterations in epithelial–mesenchymal transition (EMT), which were detected by cellular morphology and EMT protein markers, and in stemness analyzed by spheroid formation and marker molecules. Hypoxia also activated EMT, which was mediated by the nuclear factor κB (NF-κB) pathway, and stemness, and Rg3 inhibited the activation of the NF-κB pathway. Furthermore, Rg3 could increase the sensitivity to cisplatin by inhibiting EMT and stemness in hypoxic lung cancer cells, and this effect was confirmed in vivo . In conclusion, Rg3 may improve the sensitivity of cisplatin in lung cancer therapy. Highlights Hypoxia reduced cisplatin chemosensitivity in lung cancer cells. Hypoxia induced EMT and stemness mediated by the NF-κB signaling pathway. Rg3 inhibited NF-κB activation in hypoxia in a concentration/time-dependent manner. Rg3 + cisplatin inhibited hypoxia-induced EMT and stemness in vitro and in vivo . This is the first report that Rg3 had an anti-stemness effect.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  10. [해외논문]   Antiangiogenic compounds: well-established drugs versus emerging natural molecules   SCI SCIE

    Ribeiro, Andreia (Mountain Research Center (CIMO), ESA, Polytechnic Institute of Bragança, Bragança, Portugal ) , Abreu, Rui M.V. (Mountain Research Center (CIMO), ESA, Polytechnic Institute of Bragança, Bragança, Portugal ) , Dias, Madalena M. (Laboratory of Separation and Reaction Engineering –) , Barreiro, Maria Filomena (Laboratory of Catalysis and Materials (LSRE-LCM), Faculty of Engineering, University of Porto, Porto, Portugal ) , Ferreira, Isabel C.F.R. (Laboratory of Separation and Reaction Engineering –)
    Cancer letters v.415 ,pp. 86 - 105 , 2018 , 0304-3835 ,

    초록

    Abstract Angiogenesis is the natural and physiologic process of growing blood vessels from pre-existing ones. Pathological angiogenesis occurs when the precise balance of all the molecular pathways that regulate angiogenesis is disrupted, and this process is a critical step in many diseases, including cancer. A limited number of antiangiogenic synthetic drugs have been developed. However, due to toxicity and side effects issues, the search for alternative to existing drugs is ongoing. In this sense, natural molecules obtained from plants or macrofungi, have demonstrated extraordinary potential in the treatment of angiogenesis-related pathologies, specially taking into consideration its absence or very low toxicity, when compared to synthetic drugs. Using natural compounds as potential angiogenesis modulators is thus a promising field of research, supporting the creation of novel therapies able to reduce the use of drugs and associated side effects. In this review, the current status of antiangiogenic drugs and the wide variety of natural extracts and molecules with antiangiogenic capacities, as well as the angiogenesis molecular pathways and therapeutic targets, are presented. Finally, the challenges that need to be overcome in order to increase the use of natural compounds for clinical purposes are discussed. Highlights The current status of antiangiogenic drugs is presented. Natural extracts and molecules with antiangiogenic capacities are discussed. The angiogenesis molecular pathways and therapeutic targets are presented. Future challenges to increase the use of natural compounds are discussed.

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