Our previous study demonstrated that inhibition of
erythropoietin-producing
hepatoma cell line-B2 (EphB2) expression resulted in the promotion of
cancer growth, with EphB2 acting as a
tumor suppressor in
pancreatic cancer.
Qingyihuaji formula (QYHJ), a
traditional Chinese medicine, acts as an independent protective factor for
pancreatic cancer patient survival and different patients have shown various responses to QYHJ treatment. In the current study, the different effects on
tumor growth inhibition following QYHJ treatment in cells with different levels of EphB2 expression were investigated to reveal the mechanism. A subcutaneously transplanted
tumor model using
cancer cells with different levels of EphB2 expression were established in vivo and received a four-week QYHJ intervention.
Tumor weight inhibitory rate and
tumor volume deflation were evaluated. The cell cycle and apoptosis were analyzed by flow cytometry, and reverse transcription polymerase chain reaction and western blot analysis were used to assess
mRNA and
protein levels. The results showed that the
tumor weight inhibitory rate was 31.40, 31.33 and 18.36% in CFPAC-1, CFPAC-1 control RNAi and CFPAC-1 EphB2 RNAi cells following QYHJ treatment, respectively. A statistically significant difference was identified in CFPAC-1 (P<0.05) and CFPAC-1 control RNAi (P<0.01) cells. In addition, a statistically significant increase was identified in the G0/G1 phase population (P<0.05) and a statistically significant decrease was identified in the S phase population (P<0.05) in CFPAC-1 and CFPAC-1 control RNAi cells; however, no significant difference was identified in the CFPAC-1 EphB2 RNAi cells following QYHJ treatment. QYHJ upregulated the
mRNA and
protein level of
Eph receptor-interacting B1 (EphrinB1) in the cells that were expressing different levels of EphB2, however, QYHJ did not regulate EphB2 expression. In CFPAC-1 and CFPAC-1 control RNAi cells, the QYHJ treatment resulted in a statistically significant decrease in
cyclin-dependent kinase 6 (CDK6)
mRNA (P<0.05) and
protein (P<0.05) levels. The high expression of EphB2 predicted the superior response rate to the QYHJ treatment through a mechanism of inhibiting the cell cycle by an EphrinB1-EphB2-induced CDK6 decrease in CFPAC-1 cells. Therefore, EphB2 acts as a predictive factor for QYHJ treatment in
pancreatic cancer CFPAC-1 cells.