Toxins from the Caribbean sea anemone Bunodeopsis globulifera increase cisplatin-induced cytotoxicity of lung adenocarcinoma cells

Lung cancer causes 1.4 million deaths worldwide while non-small-cell lung cancer (NSCLC) represents 80-85% of the cases. Cisplatin is a standard chemotherapy against this type of cancer; however, tumor cell resistance to this drug limits its efficacy. Sea anemones produce compounds with pharmacological activities that may be useful for augmenting cisplatin efficacy. This study aimed to evaluate the pharmacological activities of crude venom (CV) from the sea anemone Bunodeopsis globulifera and four derived fractions (F1, F2, F3 and F4) to test their increase efficiency cisplatin cytotoxicity in human lung adenocarcinoma cells. Results Pre-exposure to CV, F1 and F2 fractions increases cisplatin cytotoxicity in human lung adenocarcinoma cells under specific conditions. Exposure to CV at 50 μgmL-1 induced a reduction of approximately 50% in cell viability, while a similar cytotoxic effect was observed when cell culture was exposed to F1 at 25 μgmL -1 or F2 at 50 μgmL-1. The cell culture exposure to F1 (10 μgmL-1) fraction combined with cisplatine (25 μM) provoked a decrease in MTT reduction until 65.57% while F2 (25 μgmL-1) fraction combined with cisplatin (10 μM) provoked a decrease in MTT reduction of 72.55%. Conclusions The F1 fraction had the greatest effect on the lung adenocarcinoma cell line compared with CV and F2. The combination of antineoplastic drugs and sea anemone toxins might allow a reduction of chemotherapeutic doses and thus mitigate side effects.

Toxins from the Caribbean sea anemone Bunodeopsis globulifera increase cisplatin-induced cytotoxicity of lung adenocarcinoma cells

Background: Lung cancer causes 1.4 million deaths worldwide while non-small-cell lung cancer (NSCLC) represents 80-85% of the cases. Cisplatin is a standard chemotherapy against this type of cancer; however, tumor cell resistance to this drug limits its efficacy. Sea anemones produce compounds with pharmacological activities that may be useful for augmenting cisplatin efficacy. This study aimed to evaluate the pharmacological activities of crude venom (CV) from the sea anemone Bunodeopsis globulifera and four derived fractions (F1, F2, F3 and F4) to test their increase efficiency cisplatin cytotoxicity in human lung adenocarcinoma cells. Results: Pre-exposure to CV, F1 and F2 fractions increases cisplatin cytotoxicity in human lung adenocarcinoma cells under specific conditions. Exposure to CV at 50 μgmL-1 induced a reduction of approximately 50% in cell viability, while a similar cytotoxic effect was observed when cell culture was exposed to F1 at 25 μgmL -1 or F2 at 50 μgmL-1. The cell culture exposure to F1 (10 μgmL-1) fraction combined with cisplatine (25 μM) provoked a decrease in MTT reduction until 65.57% while F2 (25 μgmL-1) fraction combined with cisplatin (10 μM) provoked a decrease in MTT reduction of 72.55%. Conclusions: The F1 fraction had the greatest effect on the lung adenocarcinoma cell line compared with CV and F2. The combination of antineoplastic drugs and sea anemone toxins might allow a reduction of chemotherapeutic doses and thus mitigate side effects.

Toxins from the Caribbean sea anemone Bunodeopsis globulifera increase cisplatin-induced cytotoxicity of lung adenocarcinoma cells.

BACKGROUND: Lung cancer causes 1.4 million deaths worldwide while non-small-cell lung cancer (NSCLC) represents 80-85% of the cases. Cisplatin is a standard chemotherapy against this type of cancer; however, tumor cell resistance to this drug limits its efficacy. Sea anemones produce compounds with pharmacological activities that may be useful for augmenting cisplatin efficacy. This study aimed to evaluate the pharmacological activities of crude venom (CV) from the sea anemone Bunodeopsis globulifera and four derived fractions (F1, F2, F3 and F4) to test their increase efficiency cisplatin cytotoxicity in human lung adenocarcinoma cells. RESULTS: Pre-exposure to CV, F1 and F2 fractions increases cisplatin cytotoxicity in human lung adenocarcinoma cells under specific conditions. Exposure to CV at 50 µgmL-1 induced a reduction of approximately 50% in cell viability, while a similar cytotoxic effect was observed when cell culture was exposed to F1 at 25 µgmL -1 or F2 at 50 µgmL-1. The cell culture exposure to F1 (10 µgmL-1) fraction combined with cisplatine (25 µM) provoked a decrease in MTT reduction until 65.57% while F2 (25 µgmL-1) fraction combined with cisplatin (10 µM) provoked a decrease in MTT reduction of 72.55%. CONCLUSIONS: The F1 fraction had the greatest effect on the lung adenocarcinoma cell line compared with CV and F2. The combination of antineoplastic drugs and sea anemone toxins might allow a reduction of chemotherapeutic doses and thus mitigate side effects.