Increased ERK phosphorylation and caveolin-1 expression on K562 human chronic myelogenous leukemia cells by jacalin, a dietary plant lectin

• Published in: Glycoconjugate journal Vol. 38; no. 3; pp. 361 - 368
• Main Authors: V, Lavanya, Jamal, Shazia, Ahmed, Neesar
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2021; Springer Nature B.V
• Subjects: AKT protein; Antineoplastic Agents, Phytogenic - pharmacology; Antitumor activity; BCR-ABL protein; Binding sites; Biochemistry; Biomedical and Life Sciences; Caveolin; Caveolin 1 - genetics; Caveolin 1 - metabolism; Caveolin-1; Chronic myeloid leukemia; Erythroleukemia; Extracellular signal-regulated kinase; Extracellular Signal-Regulated MAP Kinases - genetics; Extracellular Signal-Regulated MAP Kinases - metabolism; Fusion protein; Gene Expression Regulation - drug effects; Humans; K562 Cells; Lectins; Leukemia, Myeloid - drug therapy; Life Sciences; Membrane proteins; Membrane trafficking; mRNA; Myeloid leukemia; Pathology; Phosphorylation; Plant Lectins - chemistry; Plant Lectins - pharmacology; Short Communication; Tumorigenesis; Caveolin-1; Jacalin; PP2A; K562 cells
• ISSN: 0282-0080; 1573-4986; 1573-4986
• DOI: 10.1007/s10719-021-09998-4

The potential antitumor effects of jacalin, the plant lectin that specifically recognizes the tumor-associated Thomsen-Friedenreich antigen has been extensively studied. We had earlier reported jacalin to be mitogenic to K562, the Bcr-Abl expressing erythroleukemia cell line. The dearth of studies highlighting the proliferative effects of jacalin and other lectins motivated us to unveil the mechanism underlying the mitogenic effects of jacalin. Caveolin-1 (cav-1) is an integral membrane protein, known to play a crucial role in cell signaling, lipid transport, and membrane trafficking. The role of cav-1 in tumorigenesis is considered to be controversial as it can suppress as well as promote tumor growth, depending on the cellular context. In the present study, we propose that cav-1 plays the central role in the mitogenic effects of jacalin on the K562 cells. In accordance, the mRNA, as well as protein expression of cav-1 was found to be upregulated in the jacalin-treated K562 cells as compared to the untreated control. Further, jacalin stimulation also increased the phosphorylation of ERK and Akt. The rationale that leads to the initial conjecture about cav-1 was that the sequence of jacalin possesses a cav-1-binding site.