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Transwell results showed that the migration inhibition rates of 2.775 and 5.550MBq/ml131I-CGRRAGGSC on MDA-MB-231 and MCF-7 in breast cancer cells were (32.05 + 4.44)%, (45.92 + 2.55)% (t = 4.688, P = 0.009) and (21.99 + 1.18)%, (39.45 + 1.36)% (t = 1.36, P = 1.36).

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Through the observation of green fluorescence, it was found that HBx inhibited the production of ROS.

Western blot showed that HBx overexpression could inhibit NF- κ B (p65) and its inhibitor I κ Phosphorylation of B; NF was found after rotenone and LPS stimulated HBx overexpressing cells, respectively- κ B (p65) and its inhibitor I κ The increased phosphorylation of HMGB1, ROS and toll like receptor 4 (TLR4) suggest that HMGB1 and NF- κ There is a positive regulatory relationship between B signal pathways.

Results Western blot showed that HBx overexpression significantly inhibited the expression of HMGB1 by 2.4 times (P = 0.025).

Westernblot detected 0, 2.775, 5.550MBq/ml131I-CGRRAGGSC after treatment of breast cancer cells 24h, intracellular IL-11R α And the expression of signal transducer and activator of transcription 3 (STAT3) and phosphorylated STAT3 (p-STAT3).

Conclusion honokiol enhances the killing effect of sorafenib on hepatoma cells, and its mechanism may be related to inhibiting glycolysis and inducing apoptosis of hepatoma cells..

Methods cgrraggsc was modified with iodine labeled tyrosine by chloramine-T method; The effects of 131I-CGRRAGGSC on proliferation and migration of breast cancer cells were detected by MTT, Transwell and scratch test.

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Objective To observe the inhibitory effect of honokiol combined with sorafenib on hepatoma cell line HepG2.

α Blocking the phosphorylation of STAT3 is related.

Objective To observe the effect of hepatitis B virus X protein (HBX) expression on high mobility group protein B1 (HMGB1) and reactive oxygen species (ROS) in host cells.

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Methods HBx protein was overexpressed in normal hepatocyte line LO2; The expression of HMGB1, ROS production and nuclear factor (NF) were detected by Western blot and ROS detector DCFH-DA- κ Change of B signal pathway; Then use NF- κ Activators of B and ROS stimulated cells respectively to verify NF- κ B regulates HMGB1 and ROS.

Scratch test also confirmed that 131i-cgrraggsc inhibited MDA-MB-231 cells, but had no obvious effect on MCF-7 cells; Westernblot detection showed that with the increase of 131I-CGRRAGGSC concentration, the IL-11R in breast cancer cells treated with 24h increased.

Results 131i-cgrraggsc was successfully prepared, and its radiochemical purity was more than 95%; The inhibitory rates of 131I-CGRRAGGSC (4.625, 9.250, 18.500, 37.000MBq/ml) on the proliferation of MDA-MB-231 and MCF-7 in breast cancer cells were (21.46 + 1.08)%, (37.95 + 2.59)%, (49.18 + 0.77)%, (60.34 + 0.19)% (F = 0.19, P =%), (+ +%), (+ +%), (+ +)%, (+ +)%, (+ +%)% (F = P, = P).

(1.92 ± 0.63)] (P = 0.024), 2.5 μ After 2 days of treatment with msorafenib, the expression of ldhA in HepG2 cells increased, and the content of lactic acid in cell supernatant increased from (17.23 ± 3.42) mmol / L to (28.34 ± 8.19) mmol / L (P = 0.001); ten μ After mhonokiol combined with sorafenib, the glycolysis level of tumor cells decreased, the cell proliferation rate decreased from (74.35 ± 13.64)% to (38.16 ± 5.75)% (P = 0.008), and the apoptosis rate increased from 18% to 47% (P = 0.029).

Conclusion 131I-CGRRAGGSC can inhibit the migration of breast cancer cells, possibly with IL-11R.

Conclusion HBx inhibits NF- κ B signaling pathway, thereby inhibiting the expression of HMGB1 and the production of ROS, and inhibiting the release of inflammatory cytokines by host cells.

Objective to construct interleukin-11 receptor by chloramine-T method α( IL-11R α) The target labeled product 131i-cgrraggsc was used to observe its effect on the high expression of il-11r α Inhibition of breast cancer cells.

Methods the expression of lactate dehydrogenase A (ldhA) was detected by immunohistochemistry, the effect of sorafenib on the expression of ldhA in HepG2 cells was detected by immunofluorescence, the content of lactic acid in cell supernatant was detected by colorimetry, and the proliferation of HepG2 cells was detected by thiazole blue (MTT) test and clone formation test, Annexin V staining and caspase-3 activity test were used to detect apoptosis.

α、 P-STAT3 protein decreased gradually, but the expression of STAT3 protein did not change significantly.

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Results the expression score of ldhA in liver cancer was significantly higher than that in normal liver tissue [(3.74 ± 0.98) vs.


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