LncRNA-SNHG1 promotes macrophage M2-like polarization and contributes to breast cancer growth and metastasis.

Breast cancer is one of the most common malignant cancers among women. Cancer cells and adjacent cells determine the development of the disease. Tumor associated macrophages (TAMs) are involved in the regulation of different stages of cancer progression. LncRNAs play an important role in tumor growth and metastasis. However, the function of lncRNA in macrophage and tumor cell interaction is poorly described. Here we reported that lncRNA SNHG1 functioned as a modulator of M2 macrophage polarization and regulated tumor growth and angiogenesis. We indicated that knockdown of SNHG1 inhibited M2 macrophage polarization by suppression of STAT6 phosphorylation. SNHG1 silencing significantly alleviated migration of MCF-7 cells and tube formation of Human Umbilical Vein Endothelial Cells (HUVEC). Furthermore, we found that implantation of cell mixture of MCF-7 cells and macrophages promoted tumor growth and angiogenesis. However, knockdown of SNHG1 in macrophages reversed that effect. Collectively, we demonstrated the important role of lncRNA SNHG1 in macrophages and breast cancer cells interaction. We highlight the essential effect of lncRNA in tumor progression and provide a new method for the prevention and treatment of breast tumor metastasis.

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway.

This study aimed to investigate the effect of SIK2 on cisplatin resistance induced by aerobic glycolysis in breast cancer cells and its potential mechanism. qRt-PCR and Western blot were used to detect SIK2 mRNA and protein levels, and cisplatin (DDP) resistant cell lines of breast cancer cells were established. Viability was measured and evaluated via CCK-8, cell invasion capability was evaluated via Transwell, and apoptosis rate was assessed via Flow cytometry. The glycolysis level was evaluated by measuring glucose consumption and lactic acid production. The protein levels of p-PI3K, p- protein kinase B (Akt) and p-mTOR were determined by western blot. SIK2 was highly expressed in breast cancer tissues and cells compared with adjacent tissues and normal human breast epithelial cells, and it had higher diagnostic value for breast cancer. Silencing SIK2 expression can inhibit proliferation and invasion of breast cancer cells and induce their apoptosis. In addition, SIK2 knockdown inhibits glycolysis, reverses the resistance of drug-resistant cells to cisplatin, and inhibits PI3K/AKT/mTOR signaling pathway. When LY294002 was used to inhibit PI3K/AKT/mTOR signaling pathway, the effect of pcDNA3.1-SIK2 on aerobic glycolysis of breast cancer cells could be reversed. SIK2 can promote cisplatin resistance caused by aerobic glycolysis of breast cancer cells through PI3K/AKT/mTOR signaling pathway, which may be a new target to improve cisplatin resistance of breast cancer cells.

[Effect of topical external administration of recombinant human epidermal growth factor on expression of epidermal growth factor receptor and its mRNA in scald wound of diabetes mellitus rat].

OBJECTIVE: To investigate the effect of topical external administration of recombinant human epidermal growth factor (rhEGF) when controlling blood sugar on expression of epidermal growth factor receptor (EGFR) and EGFR mRNA of wound in diabetes mellitus (DM) combined with scald. METHODS: A total of 136 male Wistar rats weighing (188.57 +/- 6.59) g were randomly divided into 4 groups (groups A, B, C, and D, n=34). The rats was made DM model by intraperitoneal injected 60 mg/kg streptozocin in groups A, B, and C; rats were injected buffer alone in group D as control group. After 8 weeks, the rats of 4 groups were placed in 80 degrees C hot water for 6 seconds for preparation of the back deep II degree scald model. In group A, the blood sugar level was controlled at the level of group D 1 week before scald model; within 24 hours after models preparation, rhEGF was sprayed on wound at 150 U/cm2. In group B, the rats were given the same treatment as group A except not controlling blood sugar. In group C, the blood sugar was controlled as group A and wound was suture fixation with 1% silver sulfadiazine cream at 24 hours after the model. In group D, the same treatment as group A was given after injury. The healing rate of the wound was detected at 3, 7, 11, 15, and 21 days after injury; the EGFR mRNA expression was determined by mRNA hybridization in situ, and the EGFR protein expression was determined by immunohistochemistry and Western blot at 1, 3, 5, 7, 11, 15, and 21 days. RESULTS: All the rats survived at the end of experiment. There was no significant difference in the healing rate of the wound among the 4 groups at 3 days (P > 0.05). The healing rate of the wound was significantly higher in groups A and D than in groups B and C (P < 0.05) at 7, 11, 15, and 21 days. The expression of EGFR mRNA in 4 groups was observed by hybridization in situ, which mainly distributed in the dermal fibroblasts, capillary endothelial cells and remnants of skin and wound edge epithelium of the subsidiary; the expressions reached the peak at 5 days in group A, at 7 days in groups B and C, and at 11 days in group D; and the peak level was significantly higher in groups A and D than in groups B and C (P < 0.05). Immunohistochemistry and Western blot showed that the expression of EGFR protein was observed in 4 groups and reached the peak level at 7 days in groups A and B, and at 11 days in groups C and D; showing significant difference between groups B, C and groups A, D (P < 0.05). CONCLUSION: External application of rhEGF when controlling blood sugar can accelerate obviously the wound healing in DM combined with scald. After controlling blood sugar, external application of rhEGF can boost obviously the expressions of EGFR mRNA, EGFR, and the extending process of signal conduction.