Effect of bevacizumab administered prior to transarterial chemoembolization on the therapeutic effects of lenvatinib given post-TACE in primary liver cancer patients.

OBJECTIVE: To determine the therapeutic effects of lenvatinib combined with bevacizumab following transarterial chemoembolization (TACE) in patients with primary liver cancer. MATERIALS AND METHODS: 100 patients with primary liver cancer were recruited in the period from January 2020 to January 2021 and allocated with randomization into a control group (n = 50) and a test (bevacizumab) group (n = 50). The patients in the control group received lenvatinib for 4 weeks following TACE, whereas those in the test group received bevacizumab for 6 weeks prior to TACE and subsequent therapy with lenvatinib for 4 weeks. The serum concentration of interferon-γ (INF-γ), interleukin-10 (IL-10), soluble interleukin-2 receptor (sIL-2R), interleukin-12 (IL-12), superoxide dismutase (SOD), total antioxidant capacity (TAOC), glutathione (GSH), malondialdehyde (MDA), total bilirubin (TBil), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), carbohydrate antigen 242 (CA242), CA724, α-fetoprotein (AFP) and carcinoembryonic antigen (CEA) were determined in both groups at the commencement of treatment in January 2020 and 12 months later and compared with the observed therapeutic effects. RESULTS: The concentrations of CA242, CEA, CA724, and AFP in the bevacizumab group were lower than those in the control group (p < 0.05). The concentration of IL-12 and INF-γ in the bevacizumab group were higher, but the levels of IL-10 and sIL-2R lower than in the control group (p < 0.05). In the bevacizumab group, the level of MDA was lower, whereas the levels of TAOC, SOD, and GSH were higher than those in the control group (p < 0.05). The bevacizumab group also had lower levels of ALT, TBil, and AST and a higher level of ALP than control group (p < 0.05). The response rate based on tumor status (size, progression) in the bevacizumab group was higher than in the control group (p < 0.05). CONCLUSION: The therapeutic effects of lenvatinib following TACE in primary liver cancer are significantly greater when combined with bevacizumab administered for 6 weeks prior to TACE.

Expression and underlying roles of IGFBP-3 in paclitaxel-treated gastric cancer SGC-7901 cells.

PURPOSE: To study the expression of insulin-like growth factor binding proteins (IGFBPs) in paclitaxel-treated gastric cancer SGC-7901 cells, and to further investigate underlying mechanisms. MATERIALS AND METHODS: Real time PCR and Western blot assays were applied to detect the mRNA and protein expression of IGFBP-2, -3 and -5 after paclitaxel (10 nM) treatment of SGC-7901 cells. In addition IGFBP-3 expression was silenced by RNA interference to determine effects. Cell viability was determined by MTT assay. Cell cycling and apoptosis were assessed by flow cytometry. RESULTS: Compared to the control group, only IGFBP-3 expression was elevated significantly after paclitaxel (10 nM) treatment (p<0.05). Paclitaxel treatment caused cell cycle arrest and apoptosis via downregulating Bcl-2 expression. However, the effect could be abrogated by IGFBP-3 silencing. CONCLUSIONS: IGFBP-3 exhibits anti-apoptotic effects on paclitaxel-treated SGC-7901 cells via elevating Bcl-2 expression.

Sulforaphane inhibits the proliferation of the BIU87 bladder cancer cell line via IGFBP-3 elevation.

AIM: To investigate effects of sulforaphane on the BIU87 cell line and underlying mechanisms involving IGFBP-3. METHODS: Both BIU87 and IGFBP-3-silenced BIU87 cells were treated with sulforaphane. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were determined via flow cytometry. Quantitative polymerase chain reaction and Western blotting were applied to analyze the expression of IGFBP-3 and NF-κB at both mRNA and protein levels. RESULTS: Sulforaphane (80 µM) treatment could inhibit cell proliferation, inducing apoptosis and cell cycle arrest at G2/M phase. All these effects could be antagonized by IGFBP-3 silencing. Furthermore, sulforaphane (80 µM) could down-regulate NF-κB expression while elevating that of IGFBP-3. CONCLUSIONS: Sulforaphane could suppress the proliferation of BIU87 cells via enhancing IGFBP-3 expression, which negatively regulating the NF-κB signaling pathway.