Phase-Tunable Molybdenum Boride Ceramics as an Emerging Sensitive and Reliable SERS Platform in Harsh Environments.

Traditional surface-enhanced Raman scattering (SERS) sensors rely heavily on the use of plasmonic noble metals, which have limitations due to their high cost and lack of physical and chemical stability. Hence, it is imperative to explore new materials as SERS platforms that can withstand high temperatures and harsh conditions. In this study, the SERS effect of molybdenum boride ceramic powders is presented with an enhancement factor of 5 orders, which is comparable to conventional noble metal substrates. The molybdenum boride powders synthesized through liquid-phase precursor and carbothermal reduction have ß-MoB, MoB2, and Mo2B5 phases. Among these phases, ß-MoB demonstrates the most significant SERS activity, with a detection limit for rhodamine 6G (R6G) molecules of 10-9 m. The impressive SERS enhancement can be attributed to strong molecule interactions and prominent charge interactions between R6G and the various phases of molybdenum boride, as supported by theoretical calculations. Additionally, Raman measurements show that the SERS activity remains intact after exposure to high temperature, strong acids, and alkalis. This research introduces a novel molybdenum boride all-ceramic SERS platform capable of functioning in harsh conditions, thereby showing the promising of boride ultrahigh-temperature ceramics for detection applications in extreme environments.

The effect of hepatocellular carcinoma-associated fibroblasts on hepatoma vasculogenic mimicry.

Vasculogenic Mimicry (VM) is the main source of blood supply in the early stage of tumor growth. Carcinoma-associated fibroblasts (CAFs) are one of the most important host cells in the tumor microenvironment. Some studies have found that CAFs can promote tumor angiogenesis, but there are few reports on the relationship between CAFs and VM. Tissue samples were collected from 60 cases of hepatocellular carcinoma (HCC) and 10 persons with normal liver function. The relationship between VM expression and clinicopathologic features was analyzed. Furthermore, the relationship between VM expression and vimentin or α-SMA expression was analyzed. Primary culture of hepatocellular CAFs and the collection of conditioned media were carried out. The effects of hepatocellular CAF conditioned medium on the formation of VM and the levels of VM-related proteins and genes in MHCC-97H cells were studied. The positive rate of VM was 35.0% in HCC tissues. There was no VM expression in normal liver tissues. VM expression was related to tumor diameter, Edmondson grade, clinical stage, and liver cirrhosis. The expression of vimentin and α-SMA in VM-positive patients was higher than in VM-negative patients. Different concentrations of hepatocellular CAF conditioned medium could promote the formation of VM and increase the expression of VM-related genes and proteins (MMP2 and EphA2) in MHCC-97H cells. The results show that there was a significant correlation between VM formation and the expression of vimentin or α-SMA in HCC tissues. The conditioned medium of hepatocellular CAFs may promote VM formation and the expression of VM-related genes and proteins (MMP2 and EphA2) in hepatoma cell line MHCC-97H.

Effects of TGF-ß1 on the Proliferation and Apoptosis of Human Cervical Cancer Hela Cells In Vitro.

To investigate the effects of TGF-ß1 on the proliferation and apoptosis of cervical cancer Hela cells in vitro. Human cervical cancer Hela cells were cultured in vitro and divided into the experimental and control groups. In the experimental groups, Hela cells were stimulated with different concentrations of TGF-ß1 (0.01, 0.1, 1, and 10 ng/mL), while Hela cells cultured in serum-free medium without TGF-ß1 were used as controls. The CCK8 method was adopted to detect the effect of TGF-ß1 on Hela cell proliferation, and flow cytometry was used to determine cell apoptosis 72 h after TGF-ß1 treatment. Compared with the control group, the CCK-8 tests showed that different concentrations of TGF-ß1 had no obvious effect on Hela cell proliferation 24 h after treatment (P > 0.05). However, upon 48 or 72 h of treatment, TGF-ß1 significantly inhibited the proliferation of Hela cells in a time- and dose-dependent manner (P < 0.05). The flow cytometry results indicated that TGF-ß1 influenced the apoptosis of human cervical cancer Hela cells in a dose-dependent manner after 72 h of treatment (P < 0.05). TGF-ß1 significantly inhibited the growth and induced the apoptosis of human cervical Hela cells in vitro.

Effects of mTOR-STAT3 on the migration and invasion abilities of hepatoma cell and mTOR-STAT3 expression in liver cancer.

OBJECTIVE: To investigate the effects of mTOR-STAT3 pathway on the invasion and migration of hepatoma cell. METHODS: mTOR and STAT3 expression in the hepatocellular carcinoma cell line HepG2 and normal liver cell line L02 were detected by reverse transcription PCR (RT-PCR) and western blotting. The migration and invasion abilities of cells and expression of STAT3 were detected by scratch adhesion test and transwell migration assays, after siRNA transfection blocking mTOR expression of HepG2 cells. RESULTS: The HepG2 cells expression is higher compared with normal cells L02 expression. Western blotting assay showed the mTOR expression was blocked, while STAT3 expression was also decreased, after the siRNA transfection of HepG2 cells. The migration (scratch adhesion test) and invasion (transwell assays) abilities of HepG2 cells which the mTOR expression was blocked by siRNA interference were significantly decreased (P<0.05). CONCLUSION: mTORSTAT3 expression in hepatoma cells HepG2 was significantly higher than that in normal liver cells. mTOR blocking can reduce the expression of STAT3, which is also closely related to the invasion and metastasis of liver cancer cells.

Reduced expression of activin receptor-like kinase 7 in breast cancer is associated with tumor progression.

To explore the clinical implication of activin receptor-like kinase 7 (ALK7) expression in breast cancer, we evaluated its protein level in six kinds of human breast tissue samples, including adjacent normal tissues, adenosis, breast fibroadenoma, ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC), and lymph node metastases (LNM). Immunohistochemical analyses showed that ALK7 was more frequently and much more intensely expressed in adjacent normal tissues, adenosis, and fibroadenoma tissues than in malignant tissues (DCIS, IDC, and LNM). Furthermore, the ALK7 expression in primary tumors and the corresponding LNM was evaluated in parallel samples from 60 patients with IDC. Results showed that the ALK7 expression status in primary tumors and LNM was concordant in 53 patients (88%), suggesting that ALK7 expression was retained in LNM. Moreover, our results suggested that ALK7 expression inversely correlated with the tumor grade (P=0.009) and clinical stage (P=0.004) in IDC significantly. Finally, the effect of activin-ALK7 pathway on the breast cancer cell growth was elucidated, and results revealed that overexpression of ALK7 could restore the inhibitory effect of activin B on the growth of ALK7-negative breast cancer cell line, ZR-75-30. These findings provide the evidence that the reduction or lack of ALK7 expression may account for the loss of its ligand sensitivity of breast cancer cells, thereby leading to breast tumor progression.