Enhanced Anti-Cancer Effect of Snake Venom Activated NK Cells on Lung Cancer Cells by Inactivation of NF-κB

Kollipara, Pushpa Saranya; Won, Do Hee; Hwang, Chul Ju; Jung, Yu Yeon; Yoon, Heui Seoung; Park, Mi Hee; Song, Min Jong; Song, Ho Sueb; Hong, Jin Tae

doi:10.4062/biomolther.2013.103

Cited by 15 publications

(9 citation statements)

References 40 publications

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“…The present study shows that FUT2 knockdown reduces Bcl-2 expression, and increases P53 expression, which is consistent with the effect of knockdown of FUT2 on apoptosis of A549 cells. Studies showed that Bcl-2 expression might be the critical mediator allowing NF-κB-activated intestinal epithelial cells to efficiently transform [ 36 - 38 ]. Effects of sh-FUT2 on the expression of apoptosis-associated protein P65 in A549 cells suggest that NF-κB signaling pathway may play an important role in cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Clinical significance and biological function of fucosyltransferase 2 in lung adenocarcinoma

Zhou

Deng

et al. 2017

Oncotarget

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Fucosylation, which is catalyzed by fucosyltransferases (FUTs), is one of the most important glycosylation events involved in cancer. Studies have shown that fucosyltransferase 8 (FUT8) is overexpressed in NSCLC and promotes lung cancer progression. However, there are no reports about the pathological role of fucosyltransferase 2 (FUT2) in lung cancer. To identify FUT2 associated with lung cancer, the expression and clinical significance of FUT2 in lung cancer was investigated by Real-Time PCR, Immunohistochemistry and Western Blot. In addition, we investigated the effect of knockdown FUT2 in lung adenocarcinoma cells. The results showed that the expression of FUT2 in lung adenocarcinoma is higher than that in adjacent noncancerous tissues. Knocking down FUT2 in A549 and H1299 cells decreased cell proliferation, migration and invasion, and increased cell apoptosis compared to corresponding control cells. Furthermore, Western Blot showed that knockdown FUT2 can impact the expression of migration-associated and apoptosis-associated proteins in A549 cells. Our results suggest that FUT2 may be associated with lung adenocarcinoma development and thus is a potential biomarker or/and therapeutic target in lung adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

Clinical significance and biological function of fucosyltransferase 2 in lung adenocarcinoma

Zhou

Deng

et al. 2017

Oncotarget

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“…Previous trials have reported that snake venoms are able to act on the tumor in some models, such as melanoma (B16F10 cells) [21], breast (MCF-7 cells) [22], colon (HCT116 and HT-29 cells) [23], lung cancer (NCL-H460 cells) [24], and neuroblastoma (SK-N-MC and SK-N-SH cells) [25]. However, despite these data, there are few studies relating to Bothrops in cervical cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

Bothrops jararacaandBothrops erythromelasSnake Venoms Promote Cell Cycle Arrest and Induce Apoptosis via the Mitochondrial Depolarization of Cervical Cancer Cells

Bernardes-Oliveira

Gomes

Palomino

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Bothrops jararaca (BJ) and Bothrops erythromelas (BE) are viper snakes found in South-Southeast and Northeast regions of Brazil, respectively. Snake venoms are bioactive neurotoxic substances synthesized and stored by venom glands, with different physiological and pharmacological effects, recently suggesting a possible preference for targets in cancer cells; however, mechanisms of snakes have been little studied. Here, we investigated the mechanism responsible for snake crude venoms toxicity in cultured cervical cancer cells SiHa and HeLa. We show that BJ and BE snake crude venoms exert cytotoxic effects to these cells. The percentage of apoptotic cells and cell cycle analysis and cell proliferation were assessed by flow cytometry and MTT assay. Detection of mitochondrial membrane potential (Rhodamine-123), nuclei morphological change, and DNA fragmentation were examined by staining with DAPI. The results showed that both the BJ and BE venoms were capable of inhibiting tumor cell proliferation, promoting cytotoxicity and death by apoptosis of target SiHa and HeLa cells when treated with BJ and BE venoms. Furthermore, data revealed that both BJ venoms in SiHa cell promoted nuclear condensation, fragmentation, and formation of apoptotic bodies by DAPI assay, mitochondrial damage by Rhodamine-123, and cell cycle block in the G1-G0 phase. BJ and BE venoms present anticancer potential, suggesting that both Bothrops venoms could be used as prototypes for the development of new therapies.

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“…SVT has an anti-inflammatory effect [ 39 ], anti-arthritic effect [ 40 ] and anti-cancer effect [ 41 ]. Previously, we demonstrated that SVT has an anti-cancer effect of prostate [ 42 ], ovarian [ 43 ], colon [ 44 ], lung cancer [ 45 ] and neroblostoma cell [ 46 ]. SVT is actually a group of basic peptides composed of 235 amino acids with six disulfide bonds formed by 12 cysteines [ 47 ] which binds to cysteine residues of target molecules.…”

Section: Introductionmentioning

confidence: 99%

Anti-cancer effect of snake venom toxin through down regulation of AP-1 mediated PRDX6 expression

et al. 2015

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Snake venom toxin (SVT) from Vipera lebetina turanica contains a mixture of different enzymes and proteins. Peroxiredoxin 6 (PRDX6) is known to be a stimulator of lung cancer cell growth. PRDX6 is a member of peroxidases, and has calcium-independent phospholipase A2 (iPLA2) activities. PRDX6 has an AP-1 binding site in its promoter region of the gene. Since AP-1 is implicated in tumor growth and PRDX6 expression, in the present study, we investigated whether SVT inhibits PRDX6, thereby preventing human lung cancer cell growth (A549 and NCI-H460) through inactivation of AP-1. A docking model study and pull down assay showed that SVT completely fits on the basic leucine zipper (bZIP) region of c-Fos of AP-1. SVT (0–10 μg/ml) inhibited lung cancer cell growth in a concentration dependent manner through induction of apoptotic cell death accompanied by induction of cleaved caspase-3, -8, -9, Bax, p21 and p53, but decreased cIAP and Bcl2 expression via inactivation of AP-1. In an xenograft in vivo model, SVT (0.5 mg/kg and 1 mg/kg) also inhibited tumor growth accompanied with the reduction of PRDX6 expression, but increased expression of proapoptotic proteins. These data indicate that SVT inhibits tumor growth via inhibition of PRDX6 activity through interaction with its transcription factor AP-1.

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Enhanced Anti-Cancer Effect of Snake Venom Activated NK Cells on Lung Cancer Cells by Inactivation of NF-κB

Cited by 15 publications

References 40 publications

Clinical significance and biological function of fucosyltransferase 2 in lung adenocarcinoma

Clinical significance and biological function of fucosyltransferase 2 in lung adenocarcinoma

Bothrops jararacaandBothrops erythromelasSnake Venoms Promote Cell Cycle Arrest and Induce Apoptosis via the Mitochondrial Depolarization of Cervical Cancer Cells

Anti-cancer effect of snake venom toxin through down regulation of AP-1 mediated PRDX6 expression

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