Graphene oxide is a novel two-dimensional carbon nanomaterial, but it has potential risks for the health of occupationally exposed workers. This article briefly reviews the research progress on the cytotoxic mechanism of graphene oxide and its derivatives in terms of oxidative stress, physical damage and dysfunction of enzyme activity. This review also discusses effective measures for the mitigation of cytotoxicity in order to provide helpful evidence for occupational health risk and biological safety assessment of graphene nanomaterials in China.

Graphene oxide is a novel two-dimensional carbon nanomaterial, but it has potential risks for the health of occupationally exposed workers. This article briefly reviews the research progress on the cytotoxic mechanism of graphene oxide and its derivatives in terms of oxidative stress, physical damage and dysfunction of enzyme activity. This review also discusses effective measures for the mitigation of cytotoxicity in order to provide helpful evidence for occupational health risk and biological safety assessment of graphene nanomaterials in China.

Objective:To investigate the effect and mechanism of PPAR-γ agonist Pioglitazone (PGZ) on the proliferation of malignant mesothelioma (MM) cells.Methods:In December 2019, MM cell lines MSTO-211H and NCI-H2452 were incubated with different final concentrations of PGZ (0, 10, 50, 100, 150, and 200 μmol/L) for different periods of time (24 h, 48 h, and 72 h) , and then the cell proliferation level was detected by CCK8 assay. After given various final concentration of PGZ (0, 10, 50, 100, 150, 200 μmol/L) the for 72 hours, the changes of number and morphology of MM cells were observed under an inverted microscope. The expressions of PPAR-γ and HMGB1 mRNA were determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) after treatment of MM cells with PGZ of 0, 10, 50, 100 μmol/L for 72 h. The MM cells were treated with PGZ at concentration of 0, 100 μmol/L for 72 h, and the protein expressions of HMGB1 were examined using Western blotting and immunofluorescence; the protein expressions of Ki67 were assessed by immunohistochemistry.Results:The cell viability rate of MM cells was decreased after treated with PGZ ( P<0.05) . Cell number in PGZ-treated group was significantly less than that in control group and morphology changes were observed under light microscope. QRT-PCR results revealed significantly increased PPAR-γ mRNA expression in the PGZ-treated group compared to the control group ( P<0.05) . There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 μmol/L) as compared to the control group in MSTO-211H ( P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences ( P>0.05) . Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H ( P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences ( P>0.05) . Immunohistochemistry results showed increased expression of proliferation marker Ki-67. Conclusion:Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-γ.

Objective:To investigate the effect and mechanism of PPAR-γ agonist Pioglitazone (PGZ) on the proliferation of malignant mesothelioma (MM) cells.Methods:In December 2019, MM cell lines MSTO-211H and NCI-H2452 were incubated with different final concentrations of PGZ (0, 10, 50, 100, 150, and 200 μmol/L) for different periods of time (24 h, 48 h, and 72 h) , and then the cell proliferation level was detected by CCK8 assay. After given various final concentration of PGZ (0, 10, 50, 100, 150, 200 μmol/L) the for 72 hours, the changes of number and morphology of MM cells were observed under an inverted microscope. The expressions of PPAR-γ and HMGB1 mRNA were determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) after treatment of MM cells with PGZ of 0, 10, 50, 100 μmol/L for 72 h. The MM cells were treated with PGZ at concentration of 0, 100 μmol/L for 72 h, and the protein expressions of HMGB1 were examined using Western blotting and immunofluorescence; the protein expressions of Ki67 were assessed by immunohistochemistry.Results:The cell viability rate of MM cells was decreased after treated with PGZ ( P<0.05) . Cell number in PGZ-treated group was significantly less than that in control group and morphology changes were observed under light microscope. QRT-PCR results revealed significantly increased PPAR-γ mRNA expression in the PGZ-treated group compared to the control group ( P<0.05) . There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 μmol/L) as compared to the control group in MSTO-211H ( P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences ( P>0.05) . Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H ( P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences ( P>0.05) . Immunohistochemistry results showed increased expression of proliferation marker Ki-67. Conclusion:Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-γ.

Background and objective Isoliquiritigenin(ISL)is an important pharmacological constituent of Glycyrrhiza glabra,which possesses a range of physiological and pharmacological activities,as well as significant antitumor ac-tivity,and can be used as a potential drug for targeted cancer therapy.LINC01503 is an oncogene,which has been closely asso-ciated with the malignant biological processes of many cancers.The aim of this study was to investigate the effects of ISL on the proliferation,apoptosis,invasion and migration oflung squamous carcinoma cells by regulating LINC01503.Methods Plasma was collected from lung squamous carcinoma patients and healthy individuals treated at Tangshan People's Hospital from Janu-ary 2021 to December 2022.The expression of LINC01503 in lung squamous carcinoma plasma,tissues and cells was detected by real-time quantitative fluorescence polymerase chain reaction(qRT-PCR).Lung squamous carcinoma cells were treated with different concentrations of ISL for 24 h,and LINC01503 expression was detected by qRT-PCR.The cells were treated in groups:si-NC group,si-LINC01503 group,DMSO(0.1％dimethyl sulfone)group,ISL group,pc DNA3.1(+)-NC group,pc DNA3.1(+)-LINC01503 group,ISL+pc DNA3.1(+)-NC group and ISL+pc DNA3.1(+)-LINC01503 groups.CCK-8 assay,clone formation assay,flow cytometry,Transwell assay and scratch assay were used to explore the effect of LINC01503 on the functional phenotype of lung squamous carcinoma cells.Results Fluorescence in situ hybridization results showed that the average fluorescence intensity of LINC01503 in tissue microarrays of lung squamous carcinoma patients was higher than that in paracancerous tissues(P＜0.05).The expression of LINC01503 in the plasma of patients with lung squamous carcinoma was higher than that in the plasma of healthy individuals(P＜0.05).Knockdown of LINC01503 inhibited the proliferation,invasion and migration of lung squamous carcinoma cells and promoted apoptosis(P＜0.05).ISL inhibited the proliferation,invasion,migration and promoted apoptosis of lung squamous carcinoma cells(P＜0.05).Overexpression of LINC01503 followed by intervention with ISL reversed the promotional effect of overexpression of LINC01503 on the proliferation,invasion and migration of lung squamous carcinoma cells as well as the inhibitory effect on apoptosis(P＜0.05).Conclusion LINC01503 was highly expressed in lung squamous carcinoma,and LINC01503 could promote the proliferation,invasion and migra-tion of lung squamous carcinoma cells and inhibit the apoptosis,ISL could inhibit the proliferation,invasion and migration of lung squamous carcinoma cells and promote apoptosis of lung squamous carcinoma cells by regulating the expression of LINC01503.