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OBJECTIVES@#Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor of head and neck. Screening of target genes for malignant tumor therapy is one of the focuses of cancer research, with proto-oncogene and tumor suppressor gene as the breakthrough. It has become an urgent need to find the target gene related to the treatment and prognosis of LSCC.This study aims to explore the role of Lin28B and C-myc in LSCC by detecting the expressions of these two proteins and analyze the correlation between the expression of Lin28B and C-myc and clinicopathological features and prognosis of LSCC.@*METHODS@#We detected the expression of Lin28B and C-myc proteins in 102 specimens of LSCC and 90 specimens of adjacent tissues by immunochemistry, and analyzed the correlation between Lin28B and C-myc protein expressions in LSCC as well as the correlation between the expressions of the two proteins and the clinicopathological features of LSCC. At the same time, the Kaplan-Meier method was used to analyze the relation between Lin28B and C-myc protein levels with the postoperative survival rate of LSCC patients.@*RESULTS@#The protein levels of Lin28B and C-myc in the LSCC tissnes were significantly higher than those in the adjacent tissues (both P<0.05),and there was a positive correlation between the expression of Lin28B and C-myc in LSCC (r=0.476, P<0.05). The expression of Lin28B protein was closely related to age, lymph node metastasis, clinical stage, tumor size, and pathological differentiation of LSCC patients (all P<0.05). while the expression of C-myc protein was closely related to lymph node metastasis, clinical stage, tumor size, and pathological differentiation of LSCC patients (all P<0.05). A relevant survival analysis showed that in patients with higher level of Lin28B (P=0.001) or C-myc protein (P<0.001), the postoperative survival rate was relatively low.@*CONCLUSIONS@#Lin28B and C-myc proteins are highly expressed in LSCC with a positive correlation. Furthermore, they are closely related to lymph node metastasis, clinical stage, tumor size, pathological differentiation and prognosis, suggesting that both Lin28B and C-myc might be involved in the occurrence and development of LSCC.
Sujet(s)
Humains , Carcinome épidermoïde de la tête et du cou , Protéines proto-oncogènes c-myc/métabolisme , Tumeurs du larynx/diagnostic , Carcinome épidermoïde/génétique , Métastase lymphatique , Pronostic , Tumeurs de la tête et du cou , Marqueurs biologiques tumoraux/métabolisme , Protéines de liaison à l'ARN/génétiqueRÉSUMÉ
Objective To investigate the expression levels of microRNA-384(miR-384)and LIN28B in serum of patients with diabetic retinopathy(DR)and their diagnostic value.Methods A total of 100 patients with type 2 diabetes diagnosed in our hospital from January 2020 to November 2021 were selected as the research subjects.According to the occurrence of retinopathy,the patients were divided into the non-DR group(40 cases)and the DR group(60 cases).In addition,40 healthy person who underwent physical examination in our hospital during the same period were regarded as the control group.The relative expression levels of serum miR-384 and LIN28B were detected by qRT-PCR,and the relationship between the two indexes and the general clinical data of DR patients was analyzed.Pearson method was applied to analyze the correlation between the expression of miR-384 and LIN28B in serum of DR patients.Logistic regression was applied to analyze the influencing factors of DR.The diagnostic value of serum miR-384 and LIN28B levels for DR patients was analyzed by receiver operating characteristic(ROC)curve.Results The level of serum miR-384 in the DR group was obviously lower than that in the non-DR group and the control group(P<0.05),and the non-DR group was lower than the control group(P<0.05).The level of serum LIN28B in the DR group was obviously higher than that in the non-DR group and the control group(P<0.05),and the non-DR group was higher than the control group(P<0.05).The expression levels of miR-384 and LIN28B were related to the course of diabetes and blood glucose(P<0.05).Pearson's correlation analysis showed that the expression of miR-384 was negatively correlated with LIN28B in serum of DR patients(r=-0.296,P<0.05).Logistic regression analysis showed that miR-384 and LIN28B were the independent influencing factors for DR(P<0.05).The results of ROC curve analysis showed that the area under the curve(AUC)of miR-384,LIN28B and the combination of two in DR patients was 0.625,0.646,and 0.682,respectively,and the specificity was 67.50%,85.00%,and 97.50%,respectively.Conclusion The serum expression of miR-384 is low and LIN28B is high in DR patients.Both miR-384 and LIN28B are the influencing factors for the occurrence of DR and are expected to be potential serological markers for the diagnosis of DR.
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OBJECTIVE: To investigate the expression and clinical significance of Lin28 B in placenta of severe preeclampsia(SPE).METHODS: Forty SPE patients were admitted to Shengjing Hospital of China Medical University from August 2017 to August 2018,including 20 patients with early-onset severe preeclampsia(ESPE)and 20 patients with late onset severe preeclampsia(LSPE).Another 40 healthy pregnant women who had termination of pregnancy in late pregnancy due to various reasons were selected as the control group,including 20 cases in early-onset control group(N1) and 20 cases in late-onset control group(N2). RT-qPCR analysis,Western Blot analysis and immunohistochemistry were used to detect the Lin28 B expression levels in placenta of each group.RESULTS: The expression of Lin28 B in placenta was significantly lower in ESPE group than in N1 group(P0.05).The expression of Lin28 B in placenta of ESPE group was lower than that in LSPE group(P<0.05).CONCLUSION: The expression of Lin28 B in placenta of SPE patients is decreased,and the ESPE group was significantly lower than that in LSPE group,suggesting that Lin28 B may be associated with the pathogenesis and development of SPE.
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Aim To examine the role and uderlying mechanisms of Lin28 /let-7d axis in the proliferation of lung fibrobalsts and fibroblasts-into-myfibroblasts tran-sition,and provide novel strategy for the treatment of idiopathic pulmonary fibrosis (IPF).Methods We induced experimental lung fibrosis in mice by intratra-cheally injection of bleomycin (BLM).Ang Ⅱ and TGF-β1 were used to induce fibrogenesis in cultured MRC-5 cells;qRT-PCR and Western blot were applied to determine the changes of Lin28B,collagen 1 α1 and collagen 3α1 ;MTT assay,Edu satining and immun-ofluoresence were used to examine the cell viability, proliferation and fibroblasts-into-myofibroblasts transi-tion in MRC-5 cells.Results Lin28B was increased in the lung of mice with experimental lung fibrosis and in MRC-5 cells treated with AngⅡ or TGF-β1 .Moreo-ver,Lin28B enhanced collagen deposition via inhibi-ting expression of let-7d,which maybe contribute to the progression of IPF.In addition,further studies showed that Lin28B promoted proliferation and fibro-blasts-into-myofibroblasts in MRC-5 cells.Conclusion Lin28B /let-7d axis contributes to fibrogenesis via promotes fibroblasts-into-myofibroblasts transition, which may provide novel approaches for lung fibrosis treatment.
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Objective Through detected the expression degree of Lin28b in three different malig-nant degree pancreatic cancer cell lines and human pancreatic cell line to study the relationship of pancreatic cancer and the express of Lin28b.Methods The RT-PCR was used to detect the expression degree of mR-NA in Lin28b in cell lines of PANC-1,BxPC-3,AsPC-1,HPC-Y5 and Western-blot was used to detect the expression degree of protein in Lin28b in cell lines of PANC-1,BxPC-3,AsPC-1,HPC-Y5,then discovering the differential expression.Results The Lin28b was high expression in three pancreatic cancer cell lines, also higher than human pancreatic cell lines,and the expression of difference had statistical significance. Conclusions The results suggested that Lin28b may play a role in the pathogenesis of pancreatic cancer, and there is a certain relationship between the expression of Lin28b and malignant degree of tumor cells.
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Puberty onset is triggered by re-emergence of the hypothalamic-pituitary-gonadal axis (HPGA),which is characterized by the significantly increasing amplitude and frequency of gonadotropin-releasing hormone (GnRH) secretion in human being.A series of studies found that many genes control puberty onset,including KISS1 and GPR54 gene,estrogen receptor (ESR) gene,energy balance-related genes,LIN28B gene,MKRN3 gene and so on.Studies have been confirmed that the mutation and single nucleotide polymorphisms (SNP) of the genes above are associated with early puberty.In this paper,the relationship between genetic alterations of these genes and early puberty are summarized as follows.-
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Timing of puberty showed a dramatic decrease in the past decades,and it depends on the gene,nutrition,environment,social economics,and so on.Childhood obesity affects both the timing of puberty and sex hormone levels.However,the influence of obesity on the timing of puberty has gender differences.Current studies show that childhood obesity accelerates the onset of puberty in girls,but it still has controversy in boys.Mechanisms of concrete have not clear,may be related to the subjectivity of standard of male sexual development and the correlation of body mass index as a substitute for male obesity is poor.Through literature review at home and abroad,this article will explain the influence of obesity on the timing of puberty,sex hormone levels and its gender differences,further explore the possible mechanisms of body fat participate in starting the gonad axis,and provide new research direction on the switch for the gonad axis.
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To screen the differentially expressed microRNAs related to radio-resistance, we compared the microRNA profiles of lung cancer cells with different responses to ionizing radiation (IR). Of 328 microRNAs in microarray, 27 microRNAs were differentially expressed in NCI-H460 (H460) and NCI-H1299 (H1299) cells. Among them, let-7g was down-regulated in radio-resistant H1299 cells, and the level of let-7g was higher in radio-sensitive cells like Caski, H460, and ME180 in qRT-PCR analysis than in radio-resistant cells like A549, H1299, DLD1, and HeLa. Over-expression of let-7g in H1299 cells could suppress the translation of KRAS, and increase the sensitivity to IR. When we knockdown the expression of LIN28B, an upstream regulator of let-7g, the level of mature let-7g was increased in H1299 cells and the sensitivity to IR was also enhanced in LIN28B knockdown cells. From these data, we suggest that LIN28B plays an important role in radiation responses of lung cancer cells through inhibiting let-7g processing and increasing translation of KRAS.