Conditioned Media of Human Umbilical Cord Blood Mesenchymal Stem Cell-derived Secretome Induced Apoptosis and Inhibited Growth of HeLa Cells

Sandra, Ferry; Sudiono, Janti; Sidharta, Elina Ardiani; Sunata, Elisabeth Pricilia; Sungkono, Dea Jane; Dirgantara, Y.; Chouw, Angliana

doi:10.18585/inabj.v6i1.44

Cited by 18 publications

(16 citation statements)

References 20 publications

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“…(39) Meanwhile, in cancer research, modification on the microenvironment has also been reported. (40) Therefore, this potential strategy should be further investigated on ameloblastoma as well.…”

Section: Future Research Perspectivementioning

confidence: 99%

Targeting Ameloblatoma into Apoptosis

Sandra

2018

Indones Biomed J

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BACKGROUND: Generally ameloblastoma is a locally aggressive, slow growing, non-metastatic epithelial odontogenic benign tumor. However, rarely some ameloblastoma can metastasize in spite of a benign histologic appearance. Targeting ameloblastoma by inducing it into apoptosis could be a beneficial strategy, since many ameloblastoma cases were reported recurrent after surgical therapy.CONTENT: To investigate ameloblastoma in cellular aspect,cytological pattern of ameloblastoma was divided intoouter layer/peripheral and inner layer/central cells. Tumor necrosis factor (TNF)-α, Fas ligand (FasL), TNF receptor (TNFR)1/death receptor (DR)1, TNFR2/DR2, DR4, DR5andFas were highly expressed in central than peripheral cells. Despite inducing apoptosis, TNF-α can induce PI3K leading to Akt and p44/42 mitogen-activated protein kinases (MAPK) activation in AM-1 cells, which later induce cell survival and proliferation. Therefore apoptotic induction in ameloblastoma should be suggested in higher TNF-α concentration. Expression of FasL and Fas are closely associated with squamous metaplasia and granular transformation of the tumor cells, suggesting that apoptosis induced by FasL may play a role in the terminally differentiated or degenerative ameloblastoma cells. TNF-related apoptosis-inducing ligand (TRAIL) has emerged as an apoptotic inducing anticancer agent in tumor cells specifically. TRAIL induced activation of caspases, lowering mitochondrial membrane potential, high number of apoptotic cells in ameloblastoma cells. Therefore, TRAIL could be a potential agent for targeting ameloblastoma, although further study should be explored.SUMMARY: Targeting ameloblastoma by inducing it into apoptosis could be achieved effectively, although some criteria should be considered. Therefore understanding the underlying apoptosis signaling pathways are necessary for inducing ameloblasotma into apoptosis. Investigations on other apoptosis-related molecules, potential apoptosis-inducing natural products, and novel approach in reprogramming, are important in the future for a better anagement of ameloblastoma.KEYWORDS: ameloblastoma, apoptosis, TNF, Fas, TRAIL, Akt, MAPK, caspase

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Section: Future Research Perspectivementioning

confidence: 99%

Targeting Ameloblatoma into Apoptosis

Sandra

2018

Indones Biomed J

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“…Sub-G1 assay of apoptotic cells was performed as described by Sandra et al 14,15 Briefly, MG63 cells were treated with 0-10 μg/ml caffeic acid (Wako, Osaka, Japan) or chlorogenic acid (Wako, Osaka, Japan), harvested and suspended in 1 mL of hypotonic fluorochrome solution (50 μg/mL propidium iodide in 0.1% sodium citrate plus 0.1% Triton X-100). Cell suspension was placed at 4°C in the dark for 2 hours before the flow cytometric analysis.…”

Section: Sub-g1 Assaymentioning

confidence: 99%

Caffeic Acid Induced Apoptosis in MG63 Osteosarcoma Cells Through Activation of Caspases

Sandra

Sidharta

2017

Mol Cell Biomed Sci

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Background: Caffeic acid has been reported that when it is combined with all-trans retinoic acid, it can inhibit proliferation activity of SaOS-2 or OSA-01 cells. In addition, caffeic acid merely could reduce cell viability of SaOS-2 cells. However, there is not any study in caffeic acid's possible effect to induce apoptosis in osteosarcoma cell. Materials and Methods: MG-63 cells were cultured in Dulbecco's Modified Eagle Medium containing 10% fetal bovine serum. Cells were treated with various concentrations of caffeic acid. Apoptosis were analyzed with Sub-G1 assay and activation of caspase-8, -9, and -3 were analyzed with immunoblotting. Caffeic acid-induced percentage of apoptotic cells and cleaved-8, -9, -3 were then statistically analyzed. Results: Sub-G1 results showed that caffeic acid significantly induced apoptosis in MG-63 osteosarcoma cells in concentration dependent manner. Immunoblotting results showed that caffeic acid induced cleavage of caspase-8, -9 and -3. Cleavedcaspase-8 and -9 were increased at 1-hour treatment of caffeic acid, while cleaved-caspase 3 was increased markedly at 6-hours treatment of caffeic acid. Conclusion: Caffeic acid induces apoptosis significantly in concentration dependent manner through caspase-dependent intrinsic apoptotic pathway.

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“…Sub-G1 assay of apoptotic cells was performed as described by Sandra,et al(12,13) Briefly, MG63 cells were treated with 0-10 µg/ml caffeic acid (Wako, Osaka, Japan), harvested and suspended in 1 mL of hypotonic fluorochrome solution (50 µg/mL propidium iodide in 0.1 % sodium citrate plus 0.1 % Triton X-100). Cell suspension was placed at 4°C in the dark for 2 hours before the flow cytometric analysis.…”

Section: Sub-g1 Assaymentioning

confidence: 99%

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

et al. 2017

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B ACKGROUND:Caffeic acid has been shown to induce apoptosis in MG63 osteosarcoma cells. Along with the apoptotic induction, caffeic acid was shown to activate caspase-8, -9 and -3. However, the role of caspase in mediating caffeic acid-induced apoptosis in MG63 cells are not clear yet. In this study, caspase role was further investigated by inhibiting caspase activity in the caffeic acid-induced apoptosis system in the MG63 cells. METHODS:MG63 cells were cultured, starved, pretreated with/without Z-VAD FMK and treated with/without 10 µg/mL caffeic acid. To quantify the number of apoptotic MG63 cells, Sub-G1 method was performed. The caffeic acid-induced apoptotic morphology was confirmed with 4',6-diamidino-2-phenylindole (DAPI) staining and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Meanwhile, to detect apoptotic underlying mechanism, immunoblotting was performed to detect caspase-8, -9 and -3. RESULTS:The MG63 cells were significantly induced into apoptosis with the treatment of 10 µg/mL caffeic acid for 48 hours. However, pretreatment of 100 µM Z-VAD-FMK, a pan caspase inhibitor, for 2 hours, the percentage of apoptotic MG63 cells was significantly diminished. The apoptotic phenomenon induced by caffeic acid as well as the inhibition of Z-VAD-FMK were confirmed by DAPI staining and TUNEL assay. Cleaved caspase-8, -9 and -3 were formed markedly upon the treatment of caffeic acid. Pretreatment of 100 µM Z-VAD-FMK could inhibit the cleaved caspase-8, -9 and -3. CONCLUSION:Taken together, caffeic acid has the potential to induce apoptosis in MG63 cells, specifically through the caspase signaling pathway. KEYWORDS

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Conditioned Media of Human Umbilical Cord Blood Mesenchymal Stem Cell-derived Secretome Induced Apoptosis and Inhibited Growth of HeLa Cells

Cited by 18 publications

References 20 publications

Targeting Ameloblatoma into Apoptosis

Targeting Ameloblatoma into Apoptosis

Caffeic Acid Induced Apoptosis in MG63 Osteosarcoma Cells Through Activation of Caspases

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

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