Induction of apoptosis in human leukemia K562 cells by cardiotoxin III

Yang, Sheng-Huei; Lu, Mei‐Chin; Chien, Ching-Ming; Tsai, Chia-Houg; Lu, Yu‐Jhang; Hour, Tzyh‐Chyuan; Lin, Shinne‐Ren

doi:10.1016/j.lfs.2005.01.001

Cited by 34 publications

(29 citation statements)

References 22 publications

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“…The same mechanism was observed in case of drCT-I [7]. Corroborating this finding, CTX-III (Naja naja atra) also induced apoptosis in human leukemic cells by caspase 3 activation as observed by Yang et al [25].…”

Section: Discussionsupporting

confidence: 78%

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Russell’s Viper Venom Purified Toxin Drct-II Inhibits the Cell Proliferation and Induces G1 Cell Cycle Arrest in Human Leukemic Cancer Cells

AK¹

2015

Transl Med (sunnyvale)

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The present study was an effort to establish the anticancer activity of the purified protein toxin (drCT-II) from Indian Russell's viper (Daboia russelli russelli) venom in leukemic cell line and animal model. Isolation and purification of drCT-II was done through CM-cellulose ion exchange chromatography and RP-HPLC. SDS-PAGE molecular weight and first 20 amino acid sequence of drCT-II was done. The anti-leukemic activity using U937 and K562 cell line was established through cytotoxicity, apoptosis, cell cycle study, morphology, cancer marker proteins. The mean survival time of EAC induced male albino mice was established. Human lymphocyte cytotoxicity was done. drCT-II was eluted with 0.1 M NaCl on CM-cellulose ion exchange chromatography. On RP-HPLC, drCT-II produced single peak with retention time of 14.6 min. SDS-PAGE molecular weight was found to be 6.6 KDa and the first 20 amino acid sequence was found to be LQXNKLVPIASKTXPPGKNL. drCT-II produced time and dose dependent cell (U937 and K562) growth inhibition. The IC50 was found to be 35.5 µg/ml for U937 cell and 48.2 µg/ml for K562 cells. drCT-II produced membrane disruption, blebbing and nuclear disintegration in U937 and K562 cells observed through confocal and scanning electron microscopy. It exhibited DNA fragmentation and comet formation in leukemic cells. drCT-II produced apoptosis, cell cycle arrest at G 1 phase and increased the expression of P 21 , P 27 and P 53 . drCT-II induced apoptosis in leukemic cells was followed through caspase 3 and 9 pathway activation. EAC cell growth in male albino mice was significantly inhibited by drCT-II, thus increased the mean survival time. drCT-II significantly reduced the human lymphocyte count (in culture). It may be concluded that drCT-II, a 6.6 KDa protein purified from Daboia russelli russelli venom would be a novel pro-apoptotic agent that induced cancer cell killing through p53 and caspase pathway.

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Section: Discussionsupporting

confidence: 78%

“…Yang et al, identified CTX-III from Naja naja atra which showed 1.7 μg/ml IC 50 value on K562 cells and Lee et al showed cytotoxicity of OH-LAAO (isolated from King cobra) against MCF7 cell [25,26]. drCT-II induced apoptosis in both leukemic cell lines were measured by fluorescence activated cell cytometry.…”

Section: Discussionmentioning

confidence: 99%

Russell’s Viper Venom Purified Toxin Drct-II Inhibits the Cell Proliferation and Induces G1 Cell Cycle Arrest in Human Leukemic Cancer Cells

AK¹

2015

Transl Med (sunnyvale)

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“…For instance, recent studies have demonstrated that the usage of various anti-VEGF/PDGF strategies is linked to an increased risk of early metastasis in animal cancer models. Although the clinical relevance of these preclinical studies is not yet clear, these data support the idea that not only is there an imperative need to design novel anti-angiogenic drugs with better anti-invasive properties, also to test the impact of standard of care anti-angiogenics such as Avastin on metastasis [30][31][32][33][34][35][36][37][38][39][40].…”

Section: Cr Venom Of Vn Was Collected Lyophilized Successfullymentioning

confidence: 94%

“…Therefore, since 2001, the scientific research collaboration between VN and University of Southern California (USC) was established. Since 2014 this project has been approved by VN government [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40]. …”

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confidence: 99%

A Novel Anti-tumor Protein from Calloselasma Rhodostoma Venom in Vietnam

Trinh¹,

Thuc²

2016

Anat Physiol

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Aim: Vietnam is a tropical and agricultural country. Annually, there are 30,000 cases of snake bite. Two venomous snake families cause the big medical problem. In this, Calloselasma Rhodostoma (CR) is the most dangerous snake. Therefore, since 2001, the scientific research collaborations between Vietnam (VN) and University of Southern California (USC) were established. Since 2014 this project has been approved by VN government. The aims of the 1st project are to establish the technological process for purification of dsintegrin from CR venom of VN (CRd.VN), to determine the molecular weight, structure and its biological antitumor activities. Methods:The process of collection, lyophilisation of CR venom from VN. Protein concentration of CR venom was determined by BCA assay. High Performance Liquid Chromatography (HPLC), SDS-PAGE, Mass spectrometry (MS) analysis and sequencing by tryptic digestion were used for purification of CRd.VN and its molecular weight (MW) and structure. Standard cell biology methods were employed to characterize CRd's abilities (in vitro) to inhibit platelet aggregation, adhesion, migration and invasion of tumor cells. Its anti-cancer activity in a breast cancer (BC) murine model (in vivo) was tested.Results: Peak 7 of HPLC (CRd.VN), showed a single ~10 kDa band on SDS-PAGE gel. CRd.VN's MW, structure and the sequence are 7.33 kDa, a monomer containing 68 amino acids with an RGD motif (position 49-51) and 6 disulfide bonds. The anticancer activities of CRd.VN are very strong. Conclusion:We have shown that CRd.VN is a possible anti-tumor agent with clinical potential. However, further research is required on CRd recombinant production, preliminary pharmacokinetics/ toxicology properties and antitumor activities. The inhibition of angiogenesis is one of the most heavily explored treatment options for cancer, and snake venom disintegrins represent a library of molecules with different structures, potencies, and specificities and are good starting points for developing anti-angiogenesis therapeutics. Disintegrins first discovered in 1983 [11] and named in 1990 [12]. They are family of disulphide-rich, stable peptides, originally isolated from snake venom, also found in mammalian proteins (ADAMs). Disintegrins bind exclusively to activated integrins on cells, derived from multi-domain proteins by proteolytic processing, contain RGD (or alternate tri-peptide) motif at tip of a flexible 11-amino acid loop that is involved in integrin interaction. Range in size from small to medium to large and homo-and hetero-dimeric. Disintegrins hold a significant translational potential as anticancer agents based on their anti-angiogenic and anti-metastatic effects demonstrated in various experimental settings [13][14][15]. A Novel Anti-tumor Protein from Calloselasma Rhodostoma Venom in VietnamAlong with metalloproteases, disintegrins are important compounds in most Viperid and Crotalid venoms. Disintegrins represent a family of nontoxic and nonenzymatic low molecular weight (5-10 kDa) RGD-containing...

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“…Crotalus scutulatus scutulatus denominada Mojastina-1, que possui 70 aa e uma massa molecular de 7kDa (Sanchez et al, 2006) (Dufton & Hider, 1988;Yang et al, 2005;Gomes et al, 2010).…”

Section: Já Foi Demonstrado Que Uma Disintegrina Encontrada No Veneno Deunclassified

Componentes derivados de venenos de serpentes com ação antitumoral em células de melanoma Murino

Queiroz¹

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Despite the constant advances in the treatment of cancer, this disease remains one of the main causes of mortality worldwide. So, the development of new treatment modalities is imperative. Snake venom causes a variety of biological effects because they constitute a complex mixture of substances as disintegrins, proteases (serine and metalo), phospholipases A2, L-amino acid oxidases and others. The goal of the present work is to evaluate a anti-tumor activity of some snake venoms fractions. There are several studies of components derived from snake venoms with this kind of activity. After fractionation of snake venoms of the families Viperidae and Elapidae, the fractions were assayed towards murine melanoma cell line B16-F10 and fibroblasts L929. The results showed that the fractions of venom of the snake Notechis ater niger had higher specificity and potential antitumor activity on B16-F10 cell line than the other studied venoms.Since the components of this venom are not explored yet coupled with the potential activity showed in this work, we decided to choose this venom to develop further studies. The cytotoxic fractions were evaluated to identify and characterize the components that showed antitumoral activity. Western blot assays and zymography suggests that these proteins do not belong to the class of metallo and serine proteinases.

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Induction of apoptosis in human leukemia K562 cells by cardiotoxin III

Cited by 34 publications

References 22 publications

Russell’s Viper Venom Purified Toxin Drct-II Inhibits the Cell Proliferation and Induces G1 Cell Cycle Arrest in Human Leukemic Cancer Cells

Russell’s Viper Venom Purified Toxin Drct-II Inhibits the Cell Proliferation and Induces G1 Cell Cycle Arrest in Human Leukemic Cancer Cells

A Novel Anti-tumor Protein from Calloselasma Rhodostoma Venom in Vietnam

Componentes derivados de venenos de serpentes com ação antitumoral em células de melanoma Murino

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