2015
DOI: 10.1080/15384047.2015.1078021
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Abstract: To avoid cell cycle arrest or apoptosis, rapidly proliferating cancer cells have to promote DNA double strand break (DSB) repair to fix replication stress induced DSBs. Therefore, developing drugs blocking homologous recombination (HR) and nonhomologous end joining (NHEJ) - 2 major DSB repair pathways - holds great potential for cancer therapy. Over the last few decades, much attention has been paid to explore drugs targeting DSB repair pathways for cancer therapy. Here, using 2 well-established reporters for … Show more

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Cited by 35 publications
(28 citation statements)
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“…Harmine as an individual agent has been proposed to cause DNA damage, and 602 rapidly activates ATM and increases γH2AX phosphorylation without requiring ROS generation, all strongly pointing to a primary DNA damage event (Booth et al, 2014; Roberts et al, 2014; Zhang et al, 2015). One previously proposed mode of DNA repair following 602 exposure was nucleotide excision repair (NER).…”
Section: Resultsmentioning
confidence: 99%
“…Harmine as an individual agent has been proposed to cause DNA damage, and 602 rapidly activates ATM and increases γH2AX phosphorylation without requiring ROS generation, all strongly pointing to a primary DNA damage event (Booth et al, 2014; Roberts et al, 2014; Zhang et al, 2015). One previously proposed mode of DNA repair following 602 exposure was nucleotide excision repair (NER).…”
Section: Resultsmentioning
confidence: 99%
“…Harmine (C13H12ON2) is commonly distributed among the animals, marine creatures, plants, and insects (Zhang et al, 2015). Harmine derivatives are gifted with pharmacological profiles (Zhang et al, 2016).…”
Section: Structure Activity Relationshipmentioning
confidence: 99%
“…Harmine has the competency to prevent cancer progression in liver Hep3B and Huh-7 cells by inhibiting DYRK1A activity with effective inhibitory concentrations of 10 and 0.25 µM, respectively (Bruel et al, 2014;Zhang et al, 2015). Harmine has also been proved to be effective against liver HepG2, SMMC-7221, and Bel-7402 cells as it can stimulate cellular apoptosis with the activation of Bax, Fas, and caspase-3/-9 along with the down-regulating the expression of Bcl-2, and Mcl-1 (Cao et al, 2011).…”
Section: Anti-cancer Activitymentioning
confidence: 99%
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“…The search and development of herbal medicines is issue of the day [1][2][3] .Recently, scientists are attracted by natural heterocyclic compounds, which are the richest source of production of broad-spectrum drugs 4,5 .One of the most promising in the series of these compounds is the indole alkaloid harmine, which is comprehensively studied at present time [6][7][8][9][10] . According to the literature data, the neuroprotective effect 11 and the antitumor effect of harmine are discussed 12 .According to the opinion ofseveral authors 13 , harmine has great prospects, as far as an oncological drug and a combination ofharminee with an inhibitor of non-homologous end joining (NHEJ) can be an effective strategy of anticancer treatment.It has been shown that harmine can inhibit the proliferation of tumor cells and induce the arrest of the G2 / M cell cycle, accompanied by an increase in apoptotic cell death in SGC-7901 cancer cells. Harmine can exert antitumor activity at a dose of 15 mg / kg / day in vivo, which is also associated with the arrest of the cell cycle 14 .…”
Section: Introductionmentioning
confidence: 99%