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calotropin/lung neoplasms

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Calotropin from Asclepias curasavica induces cell cycle arrest and apoptosis in cisplatin-resistant lung cancer cells.

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Calotropin (M11), an active compound isolated from Asclepias curasavica L., was found to exert strong inhibitory and pro-apoptotic activity specifically against cisplatin-induced resistant non-small cell lung cancer (NSCLC) cells (A549/CDDP). Molecular mechanism study revealed that M11 induced cell

Calotropin regulates the apoptosis of non‑small cell cancer by regulating the cytotoxic T‑lymphocyte associated antigen 4‑mediated TGF‑β/ERK signaling pathway.

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Non‑small‑cell lung cancer (NSCLC) is one of the most common malignancies that is responsible for a high level of cancer‑associated mortalities worldwide. Previous evidence has shown that Calotropin is an upstream activator of protein kinase B, which can further inhibit the growth and promote the

Proceraside A, a new cardiac glycoside from the root barks of Calotropis procera with in vitro anticancer effects.

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We have studied the ethyl acetate fraction of the methanolic extract of the root barks of Calotropis procera (Asclepiadaceae) from Egypt. Bioassay-directed fractionation and final purification of the extract resulted in the identification of a new cardenolide glycoside named proceraside A (1)
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