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CdTe quantum dots with daunorubicin induce apoptosis of multidrug-resistant human hepatoma HepG2/ADM cells: in vitro and in vivo evaluation.

Zhang G, Shi L, Selke M, Wang X - Nanoscale Res Lett (2011)

Bottom Line: Apoptotic staining, DNA fragmentation, and flow cytometry analysis further demonstrated that compared with Cdte QDs or DNR treatment alone, the apoptosis rate increased after the treatment of Cdte QDs together with DNR in HepG2/ADM cells.We observed that Cdte QDs treatment could reduce the effect of P-glycoprotein while the treatment of Cdte QDs together with DNR can clearly activate apoptosis-related caspases protein expression in HepG2/ADM cells.Thus, Cdte QDs combined with DNR may serve as a possible alternative for targeted therapeutic approaches for some cancer treatments.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Lab of Bioelectronics (Chien-Shiung Wu Lab), Department of Biological Science and Medical Engineering Southeast University, Nanjing, 210096, PR China. xuewang@seu.edu.cn.

ABSTRACT
Cadmium telluride quantum dots (Cdte QDs) have received significant attention in biomedical research because of their potential in disease diagnosis and drug delivery. In this study, we have investigated the interaction mechanism and synergistic effect of 3-mercaptopropionic acid-capped Cdte QDs with the anti-cancer drug daunorubicin (DNR) on the induction of apoptosis using drug-resistant human hepatoma HepG2/ADM cells. Electrochemical assay revealed that Cdte QDs readily facilitated the uptake of the DNR into HepG2/ADM cells. Apoptotic staining, DNA fragmentation, and flow cytometry analysis further demonstrated that compared with Cdte QDs or DNR treatment alone, the apoptosis rate increased after the treatment of Cdte QDs together with DNR in HepG2/ADM cells. We observed that Cdte QDs treatment could reduce the effect of P-glycoprotein while the treatment of Cdte QDs together with DNR can clearly activate apoptosis-related caspases protein expression in HepG2/ADM cells. Moreover, our in vivo study indicated that the treatment of Cdte QDs together with DNR effectively inhibited the human hepatoma HepG2/ADM nude mice tumor growth. The increased cell apoptosis rate was closely correlated with the enhanced inhibition of tumor growth in the studied animals. Thus, Cdte QDs combined with DNR may serve as a possible alternative for targeted therapeutic approaches for some cancer treatments.

No MeSH data available.


Related in: MedlinePlus

Measurement of cellular fluorescence and drug uptake. (A) Inverted fluorescence microscopy of HepG2/ADM cells; (a) control, (b) 4 × 10-6 mol/L DNR, and (c) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR; bar, 100 μm. (B) Differential pulse voltammetry study of DNR residue outside HepG2/ADM cells after cell treatment for 2 h. (a) PBS; (b) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR treatment and cells for 2 h; and (c) 4 μM DNR. Pulse amplitude, 0.05 V; pulse width, 0.05 s; and pulse period, 0.2 s.
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Figure 3: Measurement of cellular fluorescence and drug uptake. (A) Inverted fluorescence microscopy of HepG2/ADM cells; (a) control, (b) 4 × 10-6 mol/L DNR, and (c) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR; bar, 100 μm. (B) Differential pulse voltammetry study of DNR residue outside HepG2/ADM cells after cell treatment for 2 h. (a) PBS; (b) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR treatment and cells for 2 h; and (c) 4 μM DNR. Pulse amplitude, 0.05 V; pulse width, 0.05 s; and pulse period, 0.2 s.

Mentions: Based on the above study, bio-imaging of DNR in HepG2/ADM cell lines were assayed with inverted fluorescence microscopy. For the control cells without treatment, we observed almost no intracellular fluorescence HepG2/ADM cells (Figure 3A a). DNR treatment showed relatively low fluorescence in HepG2/ADM cells (Figure 3A b). However, the intracellular fluorescence in HepG2/ADM cells increased dramatically upon treatment with DNR bound to the negatively charged surface of QDs (Figure 3A c). To understand the mechanism of this effect, electrochemical study was used to detect the interaction between DNR and HepG2/ADM cells. The results revealed that after treatment by Cdte QDs and DNR for 2 h, the peak current of the DNR residue outside HepG2/ADM cells decreased more significantly than that with DNR treatment alone, suggesting that more significant decrease of the DNR residue outside HepG2/ADM cells occurs with the treatment of Cdte QDs and DNR (Figure 3B). These observations indicate that Cdte QDs could readily facilitate the uptake of the DNR into HepG2/ADM cells.


CdTe quantum dots with daunorubicin induce apoptosis of multidrug-resistant human hepatoma HepG2/ADM cells: in vitro and in vivo evaluation.

Zhang G, Shi L, Selke M, Wang X - Nanoscale Res Lett (2011)

Measurement of cellular fluorescence and drug uptake. (A) Inverted fluorescence microscopy of HepG2/ADM cells; (a) control, (b) 4 × 10-6 mol/L DNR, and (c) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR; bar, 100 μm. (B) Differential pulse voltammetry study of DNR residue outside HepG2/ADM cells after cell treatment for 2 h. (a) PBS; (b) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR treatment and cells for 2 h; and (c) 4 μM DNR. Pulse amplitude, 0.05 V; pulse width, 0.05 s; and pulse period, 0.2 s.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3211514&req=5

Figure 3: Measurement of cellular fluorescence and drug uptake. (A) Inverted fluorescence microscopy of HepG2/ADM cells; (a) control, (b) 4 × 10-6 mol/L DNR, and (c) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR; bar, 100 μm. (B) Differential pulse voltammetry study of DNR residue outside HepG2/ADM cells after cell treatment for 2 h. (a) PBS; (b) 4 μM Cdte QDs + 4 × 10-6 mol/L DNR treatment and cells for 2 h; and (c) 4 μM DNR. Pulse amplitude, 0.05 V; pulse width, 0.05 s; and pulse period, 0.2 s.
Mentions: Based on the above study, bio-imaging of DNR in HepG2/ADM cell lines were assayed with inverted fluorescence microscopy. For the control cells without treatment, we observed almost no intracellular fluorescence HepG2/ADM cells (Figure 3A a). DNR treatment showed relatively low fluorescence in HepG2/ADM cells (Figure 3A b). However, the intracellular fluorescence in HepG2/ADM cells increased dramatically upon treatment with DNR bound to the negatively charged surface of QDs (Figure 3A c). To understand the mechanism of this effect, electrochemical study was used to detect the interaction between DNR and HepG2/ADM cells. The results revealed that after treatment by Cdte QDs and DNR for 2 h, the peak current of the DNR residue outside HepG2/ADM cells decreased more significantly than that with DNR treatment alone, suggesting that more significant decrease of the DNR residue outside HepG2/ADM cells occurs with the treatment of Cdte QDs and DNR (Figure 3B). These observations indicate that Cdte QDs could readily facilitate the uptake of the DNR into HepG2/ADM cells.

Bottom Line: Apoptotic staining, DNA fragmentation, and flow cytometry analysis further demonstrated that compared with Cdte QDs or DNR treatment alone, the apoptosis rate increased after the treatment of Cdte QDs together with DNR in HepG2/ADM cells.We observed that Cdte QDs treatment could reduce the effect of P-glycoprotein while the treatment of Cdte QDs together with DNR can clearly activate apoptosis-related caspases protein expression in HepG2/ADM cells.Thus, Cdte QDs combined with DNR may serve as a possible alternative for targeted therapeutic approaches for some cancer treatments.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Lab of Bioelectronics (Chien-Shiung Wu Lab), Department of Biological Science and Medical Engineering Southeast University, Nanjing, 210096, PR China. xuewang@seu.edu.cn.

ABSTRACT
Cadmium telluride quantum dots (Cdte QDs) have received significant attention in biomedical research because of their potential in disease diagnosis and drug delivery. In this study, we have investigated the interaction mechanism and synergistic effect of 3-mercaptopropionic acid-capped Cdte QDs with the anti-cancer drug daunorubicin (DNR) on the induction of apoptosis using drug-resistant human hepatoma HepG2/ADM cells. Electrochemical assay revealed that Cdte QDs readily facilitated the uptake of the DNR into HepG2/ADM cells. Apoptotic staining, DNA fragmentation, and flow cytometry analysis further demonstrated that compared with Cdte QDs or DNR treatment alone, the apoptosis rate increased after the treatment of Cdte QDs together with DNR in HepG2/ADM cells. We observed that Cdte QDs treatment could reduce the effect of P-glycoprotein while the treatment of Cdte QDs together with DNR can clearly activate apoptosis-related caspases protein expression in HepG2/ADM cells. Moreover, our in vivo study indicated that the treatment of Cdte QDs together with DNR effectively inhibited the human hepatoma HepG2/ADM nude mice tumor growth. The increased cell apoptosis rate was closely correlated with the enhanced inhibition of tumor growth in the studied animals. Thus, Cdte QDs combined with DNR may serve as a possible alternative for targeted therapeutic approaches for some cancer treatments.

No MeSH data available.


Related in: MedlinePlus