Melatonin and Doxorubicin synergistically induce cell apoptosis in human hepatoma cell lines

Fan, Lulu; Sun, Guoping; Wei, Wei; Wang, Zhanggui; Liu, Ge; Fu, Wei-Zheng; Wang, Hua

doi:10.3748/wjg.v16.i12.1473

Cited by 95 publications

(80 citation statements)

References 22 publications

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“…XTT activity was significantly reduced by incubation with 0.125 µM doxorubicin in HepG2 cells (60%; P=0.0075) and Hep3B cells (83%-fold; P=0.0003). The determined toxic dose ranges were comparable to previous in vitro studies using the same HCC cell lines (27)(28)(29)(30)(31)(32). Phase-contrast microscopy confirmed that, after 48 h incubation with a concentration of 1 µM doxorubicin, 10-20% of HCC cells survived (Fig.…”

Section: Selection Of Hcc Cells Surviving Doxorubicin Treatmentsupporting

confidence: 84%

Hepatocellular carcinoma cells surviving doxorubicin treatment exhibit increased migratory potential and resistance to doxorubicin re-treatment inï¿½vitro

et al. 2018

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Abstract. Transarterial chemoembolization (TACE) is an established therapeutic approach for the treatment of hepatocellular carcinoma (HCC). Although patients who undergo TACE may have prolonged survival, there are indications that the malignancy of residual HCC tissue can increase subsequent to the procedure. Although hypoxia, which occurs during TACE due to ischemia, is known to contribute to angiogenesis, little is known with regard to the undesirable effects of chemotherapeutic agents on residual HCC cells. Doxorubicin is one of the most commonly used drugs in TACE. The aim of the present study was to analyze alterations in Hep3B and HepG2 human HCC cell lines surviving doxorubicin treatment in vitro. Initially, the toxic concentration range was determined, and doxorubicin was subsequently applied in concentrations that killed >80% of the HCC cells. During the first days subsequent to treatment, surviving cells had higher expression levels of the epithelial-mesenchymal transition marker SNAIL, and exhibited increased migratory activity compared with control cells. At 3 weeks after the first doxorubicin treatment, surviving HCC cells tolerated significantly higher doxorubicin concentrations compared with control cells. As a potential explanation for this doxorubicin resistance, significantly increased mRNA expression levels of ATP-binding cassette ABCB1 (multidrug resistance protein 1) and ABCC1 (multidrug resistance-associated protein 1) were observed by reverse transcription-quantitative polymerase chain reaction. In summary, these findings indicate that, following TACE treatment, hypoxia as well as doxorubicin may induce a more malignant phenotype in surviving HCC cells and decrease susceptibility to further chemotherapeutic treatment.

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Section: Selection Of Hcc Cells Surviving Doxorubicin Treatmentsupporting

confidence: 84%

Hepatocellular carcinoma cells surviving doxorubicin treatment exhibit increased migratory potential and resistance to doxorubicin re-treatment inï¿½vitro

et al. 2018

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“…Apoptosis disorders are an additional cause for the occurrence of breast cancer. The initiation of apoptosis is typically triggered via caspase-3 (39), which is being used to treat cancer; for example, a number of chemotherapeutic drugs, including melatonin, doxorubicin and cisplatin, induce cancer cell apoptosis by upregulating the activity of caspase-3 (40,41). Therefore, novel drugs, which repress Akt signaling or increase caspase-3 activity, may be effective tools to improve breast cancer prognosis.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine regulates breast cancer cell viability, migration, invasion and apoptosis by affecting the activity of Akt and caspase-3

Shen¹,

Zeng²,

Pan³

et al. 2018

Oncol Lett

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Abstract. Tetramethylpyrazine (TMP), an effective component of the traditional Chinese medicine Chuanxiong Hort, has been proven to exhibit a beneficial effect in a number of types of malignant epithelial cancer. However, the mode of action of TMP on breast cancer cells remains unknown. The aim of the present study was to investigate the regulatory effect of TMP on breast cancer cells and its underlying molecular mechanism of action. Different concentrations of TMP were used to treat breast cancer cells, and subsequently, the effects on the viability, apoptosis, and migration and invasion abilities were determined. In addition, the expression and activity levels of the protein kinase B (Akt) signaling pathway and caspase-3 were explored via reverse transcription-quantitative polymerase chain reaction and western blot analysis. The results of the present study revealed that TMP significantly inhibited the viability, migration and invasion rates, and increased the apoptosis of MDA-MB-231 cells in a dose-dependent manner. The minimum effective dose was ~1,600 µM. Additional mechanistic studies demonstrated that 1,600 and 3,200 µM TMP significantly decreased the gene expression and activity of Akt and increased the activity of caspase-3. This mechanism may be responsible for the inhibition of viability, migration and invasion, and activation of apoptosis in breast cancer cells. The results of the present study suggested that TMP may be used in chemotherapy against breast cancer.

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“…et al, 1999), SK-N-MC (human neuroblastoma cell line) (Garcia-Santos et al, 2006), B65 (rat dopaminergic neuroblastoma cell line) (Pizarro et al, 2008), AR42J (rat pancreatic tumor cell line) (Uguz et al, 2012), HepG2 (hepatocarcinoma cell line) (Martin-Renedo et al, 2008;Fan et al, 2010), LnCaP (prostate cancer cell line) (Joo and Yoo, 2009), HL60 (human leukemia cell line), Jurkat (human T lymphoblastic leukemia cell line), MOLT-4 (human T lymphoblastic leukemia cell line), Daudi (human B lymphoblastic cell line), K562 (erythroleukemia cell line) (Büyükavcı et al, 2006), SNG-II (human uterine endometrial adenocarcinoma cell line), and Ishikawa (human endometrial adenocarcinoma cell line) (Kanishi et al, 2000) cell lines. Our results showed that melatonin inhibited cell viability in 5RP7 cells, and growth inhibition of the melatonin (380 µM) was both dose-and time-dependent for 24 and 48 h. However, this cytotoxic effect was not observed in the NIH/3T3 cells at this concentration.…”

Section: Controlmentioning

confidence: 99%

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

Kaplan

Çiftçi²,

Kutlu³

2015

Turk J Biol

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IntroductionOncogenes are important factors in the carcinogenesis process. Cancer cells may demonstrate an uncontrolled proliferation due to oncogenes. Ras is one of these oncogenes, and it is responsible for cell differentiation/ proliferation. It is well known that ras mutation occurs in human tumors such as pancreatic, thyroid, and colon cancers. H-ras, K-ras, and N-ras proteins belonging to the ras family play a role in cancer diseases (Brunner et al., 2004). Thus, ras genes are effective targets for anticancer drug development (Weiwer et al., 2012). In this study, we used H-ras oncogene transformed 5RP7 cells. These cells were obtained from embryonic tissues of Rattus norvegicus and transformed by the H-ras oncogene.Melatonin (N-acetyl-5-methoxytryptamine) is a methoxyindole secretory product as a natural compound, which is produced by the pineal gland and a variety of organs (such as the retina, Harderian glands, gut, ovary, testes, or bone marrow) during the dark phase (Leon-

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Melatonin and Doxorubicin synergistically induce cell apoptosis in human hepatoma cell lines

Abstract: The synergism of melatonin and doxorubicin inhibits hepatoma cell growth and induces cell apoptosis.

Cited by 95 publications

References 22 publications

Hepatocellular carcinoma cells surviving doxorubicin treatment exhibit increased migratory potential and resistance to doxorubicin re-treatment inï¿½vitro

Hepatocellular carcinoma cells surviving doxorubicin treatment exhibit increased migratory potential and resistance to doxorubicin re-treatment inï¿½vitro

Tetramethylpyrazine regulates breast cancer cell viability, migration, invasion and apoptosis by affecting the activity of Akt and caspase-3

Melatonin induces antiproliferative activity through modulation of apoptoticpathway in H-ras oncogene transformed 5RP7 cells

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