Abstract: Purpose: To explore the role and molecular mechanism of proteins secreted by L. acidophilus CICC6005 in promoting intestinal health and to reveal that this topic is well worth further investigation. Methods: This experiment determined extracellular proteins secreted by L. acidophilus CICC6005 to inhibit the proliferation of HT-29 cells and further explored the pathway by which the extracellular proteins 67 and 37 ku inhibited tumor proliferation. In the present study, HT-29 cells were used as target cells to evaluate the expression levels of the critical target protein p38, c-Jun N-terminal kinase (JNK), c-Jun N-terminal kinase (ERK), phosphorylated p38 (p-p38), phosphorylated c-Jun N-terminal kinase (p-JNK), phosphorylated extracellular signal-regulated kinase (p-ERK), phosphorylated protein kinase B (p-AKT), phosphatidylinositol-3-kinase (PI3K) in the mitogen activated protein kinase (MAPK) and (phosphatidylinositol 3-kinase-protein kinase B) PI3K-AKT signaling pathways through Western blotting in order to explore the molecular mechanism by which that the extracellular proteins from L. acidophilus CICC6005 regulated the proliferation of colon cancer cells. Results: Exposure of HT-29 cells to different concentrations of 67 and 37 ku extracellular proteins from L. acidophilus CICC6005 could significantly inhibit the expression of p-ERK1/2, p-p38, p-AKT and PI3K in a dosedependent manner for both signaling pathways but not the expression of p-JNK, ERK1/2, p38 and JNK. Conclusion: The extracellular proteins 37 and 67 ku from L. acidophilus CICC6005 could inhibit the proliferation of HT-29 cells, and the mechanism might be related to the activation level of the critical proteins involved in the MAPK and PI3K-AKT pathways. Consumption of extracellular proteins from L. acidophilus could help to maintain intestinal health.

Key words: Lactobacillus acidophilus CICC6005, extracellular proteins, colon cancer cell line HT-29, mitogen activated protein kinase (MAPK), phosphatidylinositol-3-kinase/protein kinase B (PI3K-AKT)