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Journal of Cancer Research Updates

In Vitro Evaluation of the Antiinflammatory and Anticancer Activities of Compounds from the Plants Casearia sylvestris and Zanthoxylum monophyllum
Pages 114-121
Omar A. Dupuy L., José A. Bonilla V., Renato Murillo M., Peter Taylor, María J. Abad, Lorena I. González P., Olmedo Otero and Johanna Juliao A.

DOI: http://dx.doi.org/10.6000/1929-2279.2015.04.03.2

Published: 13 August 2015

 


Abstract: The anthocyanins, coumarins, and casearins are interesting compounds due to their chemical and biological properties. In the present study, the in vitro effect of 4´-O-methyl-gallocatechin (an anthocyanin), columbianatin (a coumarin), and casearin G on the mitogenic response and phagocytic activity from whole blood cells, was evaluated. In addition, the cytotoxic effect of these compounds on the cell lines B16/BL6 (murine melanoma) and COS-7 (kidney fibroblasts transfected with SV40 virus) was measured by a colorimetric assay (MTS/PMS, IC50: inhibitory concentration) and the sulphorhodamine B assay (GI50: growth inhibition, TGI: total growth inhibition, LC50: lethal concentration). The results show that 4´-O-methyl-gallocatechin and columbianatin reduced lymphoproliferation. Columbianatin reduced both the phagocytic index and the percentage of phagocytic monocytes/macrophages. Casearin G showed both cytotoxic (IC50, LC50) and cytostatic (GI50) effects against the tumor cells, B16/BL6 (IC50 = 30.8 μM; GI50 = 12.4 μM; LC50 = 34.7 μM) and COS-7 (IC50 = 137.3 μM; GI50 = 3.8 μM; LC50 = 29.9 μM). In conclusion, 4´-O-methyl-gallocatechin and columbianatin showed immunosuppressive properties in vitro while casearin G was the most cytotoxic.

Keywords: 4´-O-methyl-gallocatechin, columbianatin, casearin G, peripheral blood mononuclear cells, B16/BL6 melanoma, COS-7.

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Journal of Cancer Research Updates

Human Chorionic Gonadotropin (hCG) Testing in Specimens of Tumor and Myometrial Tissues During Surgical Treatment of Gestational Trophoblastic Tumors
Pages 122-126
Reda Hemida, Mohammad Arafa, Hosam AbdElfattah and Doaa Sharaf-Eldin

DOI: http://dx.doi.org/10.6000/1929-2279.2015.04.03.3

Published: 13 August 2015


Abstract: Background: Gestational trophoblastic tumors originate from trophoblastic tissues and secrete human chorionic gonadotrophin (hCG). Surgical treatment may be a line of treatment of chemoresistant cases.

Objective: To evaluate the accuracy of hCG dipsticks in detection of hCG in tissues of trophoblastic tumors and healthy myometrium during surgery of trophoblastic tumors.

Methods: We included 19 samples of tumor and apparently healthy myometrial tissues during surgical treatment of 5 cases of gestational trophoblastic tumors. The hCG dipstick was immersed in a solution containing 1x1 cm of tumor or myometrial tissues. The results of the tests were compared to the histopathological results.

Results: The mean age of patients were 38.8 years, the mean parity was 3.4. The mean serum B-hCG level was 101,745.6 mu/ml. Except for one specimen in case 5, all results of the hCG dipsticks were concordant with final histopathologic analysis of the specimens. Sensitivity of hCG test was 100% and specificity was 90%.

Conclusion: Intraoperative detection of hCG in different tissues and suspicious masses can be considered as simple, rapid, inexpensive, and reliable test. It can be used to detect the trophoblastic nature of tissues if frozen section is not available as some low resource setting countries. We recommend further larger prospective studies to compare the accuracy and reliability of this novel technique and frozen section analysis.

Keywords: Trophoblatic tumors, surgery, hCG test.

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Journal of Cancer Research Updates

Metabolic Imbalance Associated Mitophagy in Tumor Cells: Genesis and Implications
Pages 95-107
Madhuri Chaurasia, Shashank Misra, Anant N. Bhatt, Asmita Das, Bilikere Dwarakanath and Kulbhushan Sharma

DOI: http://dx.doi.org/10.6000/1929-2279.2015.04.02.8

Published: 13 May 2015

 


Abstract: Emerging knowledge supports the notion that metabolic reprogramming facilitates the progression of many cancers and in some it could be initiated by mutations in genes related to mitochondrial function. While dysfunctional mitochondria plays a pivotal role in driving metabolic reprogramming, mitophagy that recycles damaged mitochondria by selective and organized degradation appears to be vital for sustaining carcinogenesis. Although the potential of targeting mitophagy as a therapeutic strategy has still remained elusive, poor prognosis and therapeutic resistance of highly glycolytic tumors suggest that inhibitors of mitophagy could be potential adjuvant in radio- and chemotherapy of tumors. We briefly review the current status of knowledge on the interrelationship between mitophagy and metabolic reprogramming during carcinogenesis and examine mitophagy as a potential target for developing anticancer therapeutics and adjuvant.

Keywords: Warburg, PARKIN, Oxidative stress, Metabolic Reprogramming, Calcium.

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Journal of Cancer Research Updates

Bufalin Induces Apoptosis of MDA-MB-231 Cell Through Activation of JNK/p53 Pathway
Pages 47-53
Jian-Yang Hu, Min-Feng Chen, Xue-Ping Lei, Zhen-Jian Zhuo, Hai-Yan Sun, Zhe-Sheng Chen, Zhi Shi, Dong-Mei Zhang and Wen-Cai Ye

DOI: http://dx.doi.org/10.6000/1929-2279.2015.04.02.1

Published: 07 May 2015

 


Abstract: Cinobufacini has been widely used at oncology clinics in China to treat many kinds of cancers and bufalin is one active compound of it, but the anti-cancer effect and the underlying mechanisms of bufalin on breast cancer cells are still unclear. Our study demonstrated that bufalin could effectively decrease the viability of MDA-MB-231 cells with IC50 values of 152.2 ± 8.0 nM for 24 h and 22.4 ± 2.3 nM for 48 h, respectively. Further study showed that bufalin could trigger MDA-MB-231 cells to undergo apoptosis with up-regulating protein expression of p-JNK/JNK, p53, p-ERK/ERK, Puma and down-regulating protein expression of Bcl-2, supporting the possible application of bufalin to breast cancer treatment.

Keywords: Apoptosis, JNK, p53, Bcl-2, MDA-MB-231 cell.

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