Retraction Note: Novel piperazine core compound induces death in human liver cancer cells: possible pharmacological properties

Samie, Nima; Muniandy, Sekaran; Kanthimathi, M.S.; Haerian, Batoul Sadat; Azudin, Raja Elina Raja

doi:10.1038/srep29056

Cited by 4 publications

(3 citation statements)

References 2 publications

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“…The mitochondria is a major source of ROS in cells, and these chemicals regulate cell viability or mortality 29,30. Although oxygen metabolism is central to life, beyond the cellular antioxidant capacity, it has been reported to damage macromolecular structures and to induce apoptosis of cancer cells 17,31,32. In this study, ROS production in Artonin E-treated MCF-7 cells was significantly ( P <0.05) enhanced.…”

Section: Discussionmentioning

confidence: 99%

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Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells

Etti¹,

Abdullah²,

Hashim³

et al. 2017

DDDT

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Artonin E is a prenylated flavonoid compound isolated from the stem bark of Artocarpus elasticus. This phytochemical has been previously reported to be drug-like with full compliance to Lipinski’s rule of five and good physicochemical properties when compared with 95% of orally available drugs. It has also been shown to possess unique medicinal properties that can be utilized in view of alleviating most human disease conditions. In this study, we investigated the cytotoxic mechanism of Artonin E in MCF-7 breast cancer cells, which has so far not been reported. In this context, Artonin E significantly suppressed the breast cancer cell’s viability while inducing apoptosis in a dose-dependent manner. This apoptosis induction was caspase dependent, and it is mediated mainly through the intrinsic pathway with the elevation of total reactive oxygen species. Gene and protein expression studies revealed significant upregulation of cytochrome c, Bax, caspases 7 and 9, and p21 in Artonin E-treated MCF-7 cells, while MAPK and cyclin D were downregulated. Livin, a member of the inhibitors of apoptosis, whose upregulation has been noted to precede chemotherapeutic resistance and apoptosis evasion was remarkably repressed. In all, Artonin E stood high as a potential agent in the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

“…Aliquots of cell suspension (20 µL) were examined under Carl Zeiss Axioskop plus-2 fluorescence microscope. At least 200 cells in each of three fields were immediately assessed for viability, early and late apoptosis, as well as necrosis 17. The experiment was done in triplicates.…”

Section: Methodsmentioning

confidence: 99%

Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells

Etti¹,

Abdullah²,

Hashim³

et al. 2017

DDDT

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“…TXER + Cu complex significantly caused apoptosis related changes by inducing ROS generation. Apoptosis related cell death consists of morphological and biochemical changes (Samie, Muniandy, Kanthimathi, Haerian, & Azudin, ). Following the death indication, morphological occurrences instigated by cell shrinkage, chromatin condensation, and nuclear fragmentation and lastly end with apoptotic development.…”

Section: Discussionmentioning

confidence: 99%

Troxerutin with copper generates oxidative stress in cancer cells: Its possible chemotherapeutic mechanism against hepatocellular carcinoma

Subastri

Arumugam

Babu

et al. 2017

Journal Cellular Physiology

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Troxerutin (TXER) a rutin derivative is known for its anticancer effect against hepatocellular carcinoma (HCC). As part of large study, recently we have shown TXER interact with genetic material and its anti-mutagenic property. In the present study we have explored its possible mode of action in HCC. Since TXER alone did not show significant anticancer effect on Huh-7 cells, in vitro biochemical assays were performed for determining anticancer efficacy of TXER + metal complex using transition metals such as Cu, Zn, and Fe. The anticancer efficacy of TXER + Cu on Huh-7 cells were evaluated using MTT assay, DCFDA, JC-1 staining, comet assay, cell cycle analysis, immunocytochemistry, and Western blotting. Non-toxic nature of TXER was analyzed on primary rat hepatocytes. The in vivo efficacy of TXER was tested in N-nitrosodiethylamine initiated and γ-benzene hexachloride and partial hepatectomy promoted rat liver cancer. Liver markers, transition metal levels, histopathological examination, and expression levels of GST-P, 8-OHdG and Ki-67 were studied to assess the in vivo anticancer effect of TXER. We observed that TXER + Cu induced extensive cellular death on Huh-7 cells through generating free radicals and did not possess any toxic effect on normal hepatocytes. The in vivo studies revealed that TXER possess significant anti-cancer effect as assessed through improved liver markers and suppressed GST-P, 8-OHdG, and Ki-67 expression. TXER treatment reduced the hepatic Cu level in cancer bearing animals. Current study brings the putative mechanism involved in anti-cancer effect of TXER, further it will help to formulate phytoconstituents coupled anti-cancer drug for effective treatment of HCC.

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Nickel(II) bis(isatin thiosemicarbazone) complexes induced apoptosis through mitochondrial signaling pathway and G0/G1 cell cycle arrest in IM-9 cells

Balachandran

Haribabu

Jeyalakshmi

et al. 2018

Journal of Inorganic Biochemistry

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Retraction Note: Novel piperazine core compound induces death in human liver cancer cells: possible pharmacological properties

Cited by 4 publications

References 2 publications

Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells

Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells

Troxerutin with copper generates oxidative stress in cancer cells: Its possible chemotherapeutic mechanism against hepatocellular carcinoma

Nickel(II) bis(isatin thiosemicarbazone) complexes induced apoptosis through mitochondrial signaling pathway and G0/G1 cell cycle arrest in IM-9 cells

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