Lectin isolated from Abelmoschus esculentus induces caspase mediated apoptosis in human U87 glioblastoma cell lines and modulates the expression of circadian clock genes.

Lectins are a cluster of proteins which are capable of recognizing and binding to glycoconjugates and are extensively found in plants, animals, fungi and bacteria. Plant-derived lectins have been gaining importance over the years due to their innumerable biological activities and also have the added possibility of being compatible to the human system while simultaneously exhibiting properties like antimicrobial and antitumor activities. Abelmoschus esculentus (AE) commonly known as okra is a vegetable with medicinal properties. AE extracts are used to treat disorders such as constipation, microbial infection, urine retention, hypoglycemia and inflammation in humans. Previous studies showed that lectin isolated from AE exhibited anti inflammatory, anti nociceptive, anticancer, antioxidant and hemagglutinating activities. However, the antitumor effect of the lectin derived from this plant against neural cancer cells still remains unexplored. Glioblastoma is a malignant tumor of the nervous system. Treatment options for patients afflicted by glioblastoma is limited to surgical resection, preceded by radiation therapy and followed by chemotherapy. Hence it would be of interest to identify novel bio molecules with ability to selectively target glioblastoma with minimum side effects. In this aspect, lectins from vegetables that are commonly used as food products could offer a promising lead as anticancer molecules. The present study proves the anti-proliferative effect of lectin isolated from AE on human U87 glioma cells. MTT assay showed significant concentration dependent cytotoxic activity and the IC value was calculated as 21 μg/ml. Further, annexin V/FITC staining by FACS, the expression of caspase 3 and 7 and the circadian genes clock and Bmal1 using RT-PCR and the generation of intracellular ROS, cell cycle analysis by FACS revealed the ability of AEL to induce effective apoptosis.