Blood Vessels ; physiology ; Humans ; Kruppel-Like Transcription Factors ; metabolism ; physiology

Overexpression of Krüppel like factor 2 (Klf2) or Klf7 inhibits adipocyte formation. However, it remains unclear whether Klf2 regulates klf7 expression in adipose tissue. In this study, oil red O staining and Western blotting were employed to study the effect of Klf2 overexpression on the differentiation of chicken preadipocytes. The results showed that Klf2 overexpression inhibited the differentiation of chicken preadipocytes induced by oleate and the expression of pparγ, while promoted klf7 expression in chicken preadipocytes. Spearman correlation analysis was used to study the correlation between the expression data of klf2 and klf7 in the adipose tissue of both human and chicken. The results showed that there was a significantly positive correlation between the expression of klf2 and klf7 in adipose tissues (r > 0.1). Luciferase reporter assay showed that overexpression of Klf2 significantly promoted the activity of chicken klf7 promoter (-241/-91, -521/-91, -1 845/-91, -2 286/-91, -1 215/-91; P < 0.05). In addition, the activity of klf7 promoter (-241/-91) reporter in chicken preadipocytes was significantly positively correlated with the amount of klf2 overexpression plasmid transfected (T_au=0.917 66, P=1.074×10^-7). Moreover, Klf2 overexpression significantly promoted the mRNA expression of klf7 in chicken preadipocytes (P < 0.05). In conclusion, upregulation of klf7 expression might be one of the pathways that Klf2 inhibits chicken adipocyte differentiation, and the sequence from -241 bp to -91 bp upstream chicken klf7 translation start site might mediate the regulation of Klf2 on klf7 transcription.
Animals ; Humans ; Chickens/genetics* ; Kruppel-Like Transcription Factors/metabolism* ; Transcription Factors/metabolism* ; Adipocytes/metabolism* ; Adipose Tissue/metabolism*

Krüppel-like factor 7 (KLF7), a member of Krüppel-like transcription factors (KLFs), also known as ubiquitous Krüppel- like factor (UKLF), is ubiquitously expressed in various tissues of adult human beings. Genetics reports showed that the genetic polymorphism of KLF7 is associated with obesity, type 2 diabetes, mental development in human beings; and KLF7 methylation is associated with the development of diffuse gastric cancer (gastric adenocarcinoma). In addition, some genomics reports suggested that KLF7 is one of the key transcription factors in the regulatory networks of serum markers change during the cardiovascular disease. The function studies showed that KLF7 is involved in the regulation of the development and function of the nervous system and adipose tissue, type 2 diabetes, blood diseases, as well as pluripotent cells maintenance. This review summarizes the research progress of KLF7 in genetic characteristics, protein structure and gene function.
Diabetes Mellitus, Type 2 ; Humans ; Kruppel-Like Transcription Factors ; metabolism ; Nervous System ; Obesity

To investigate the expression of KLF6mRNA in primary hepatocellular carcinoma (HCC), nomal liver tissues and the tissues adjacent to the cancers, reverse-transcription polymerase chain reaction (RT-PCR) was employed to investigate the expression of the KLF6 gene in HCC, the corresponding adjacent non-cancerous tissues and normal liver tissue. Our results showed that an amplified fragment of 427 bp DNA was detected in 18 of 19 (94.7%) adjacent non-cancerous tissues and normal liver tissue, and in 12 (85.7%) of 14 HCC. There were no significant differences in the levels of KLF6 mRNA between normal liver and liver tumors (P>0.05). It is concluded that KLF6 mRNA is generally expressed in HCC.
Carcinoma, Hepatocellular/*metabolism ; Kruppel-Like Transcription Factors/*biosynthesis ; Kruppel-Like Transcription Factors/genetics ; Liver/metabolism ; Liver Neoplasms/*metabolism ; Proto-Oncogene Proteins/*biosynthesis ; Proto-Oncogene Proteins/genetics ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo study the effects of rosiglitazone on Kruppule-like factor 6 (KLF6) and its target gene TGFâ1 during the development of nonalcoholic fatty liver fibrosis.

METHODThirty-six Wistar rats were divided into three groups: a control group, a high fat model group and an intervention group. Their blood serum TG, FFA, AST, ALT, HA, LN and CIV were measured. Hepatic expressions of KLF6, TGFbeta1 and alpha-SMA were detected by RT-PCR and immunohistochemistry. The pathological features and the degree of liver fibrosis before and after the rosiglitazone intervention were also studied.

RESULTSThe contents of TG, FFA, AST, ALT, HA, LN and CIV, the expression of KLF6, TGFbeta1 and alpha-SMA mRNA, and the degree (score) of liver fibrosis at the 24th week in the model group were significantly higher than those in the control group (P<0.01) but they were lower in the rosiglitazone intervention group (P<0.05). The protein expression of a-SMA was also lower in the intervention group compared with that of the model group.

CONCLUSIONRosiglitazone, to a certain extent, can inhibit KLF6-TGFbeta1 signal transduction by inducing expression of PPAR-gamma, and then inhibit the activation of hepatic stellate cells and minimize hepatic fibrosis.

Animals ; Fatty Liver ; metabolism ; pathology ; Kruppel-Like Factor 6 ; Kruppel-Like Transcription Factors ; metabolism ; Liver ; metabolism ; Male ; PPAR gamma ; metabolism ; Proto-Oncogene Proteins ; metabolism ; Rats ; Rats, Wistar ; Signal Transduction ; drug effects ; Thiazolidinediones ; pharmacology ; Transforming Growth Factor beta1 ; metabolism

To investigate the expression of KLF6mRNA in primary hepatocellular carcinoma (HCC), nomal liver tissues and the tissues adjacent to the cancers, reverse-transcription polymerase chain reaction (RT-PCR) was employed to investigate the expression of the KLF6 gene in HCC, the corresponding adjacent non-cancerous tissues and normal liver tissue. Our results showed that an amplified fragment of 427 bp DNA was detected in 18 of 19 (94.7%) adjacent non-cancerous tissues and normal liver tissue, and in 12 (85.7%) of 14 HCC. There were no significant differences in the levels of KLF6 mRNA between normal liver and liver tumors (P>0.05). It is concluded that KLF6 mRNA is generally expressed in HCC.
Carcinoma, Hepatocellular ; metabolism ; Humans ; Kruppel-Like Factor 6 ; Kruppel-Like Transcription Factors ; biosynthesis ; genetics ; Liver ; metabolism ; Liver Neoplasms ; metabolism ; Proto-Oncogene Proteins ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction

Animals ; Astrocytes ; cytology ; Cell Differentiation ; Cellular Reprogramming ; Induced Pluripotent Stem Cells ; cytology ; Kruppel-Like Transcription Factors ; genetics ; metabolism ; Mice ; Neurons ; cytology ; Octamer Transcription Factor-3 ; genetics ; metabolism

The aim of this study was to investigate the effect of TIEG1 on K562 cell apoptosis and expression of BCL-2/BAX, PTEN. The different concentration(0, 1, 5, 10, 20 ng/ml) of TIEG1 were used to treat K562 cells, the cell growth inhibition rate was detected by using MTT method. After treating K562 cells with 10.00 ng/ml TIEG1, the cell apoptosis was detected with flow cytometry. The RT-PCR was used to detected the expression levels of BCL-2 /BAX and PTEN. The results showed that TIEG1 displays inhibitory effect on proliferation of K562 cells in time-and dose-dependent manner (r = 0.52, P < 0.05) ; after K562 cells were treated for 6, 12, 24 and 48 h, the IC50 of TIEG1 were 48.19, 18.72, 9.5 and 3.85 ng/ml respectively. After treating K562 cells with 10.00 ng/ml TIEG1 for 0, 6, 12, 24, 48 h, the apoptosis rate were (2.13 ± 0.42)%, (7.79 ± 0.71)%, (11.17 ± 1.37)%, (24.66 ± 0.29)% and (48.60 ± 1.38)% respectively, and there was significant difference between groups(P < 0.05). In process of K562 cell apoptosis, the expression level of BCL-2 gradually decreased (r = 0.48, P < 0.05), meanwhile the expression levels of BAX (r = 0.69, P < 0.05) and PTEN (r = 0.57, P < 0.05) gradually increased. It is concluded that TIEG1 can indue apoptosis of K562 cells and inhibit K562 cell proliferation in time-and dose-dependent manner. In apoptosis process of K562 cells induced by TIEG1, the expression changes of BCL-2/BAX and PTEN associate with the K562 cell apoptosis.
Apoptosis ; Cell Proliferation ; Humans ; K562 Cells ; Kruppel-Like Transcription Factors ; metabolism ; PTEN Phosphohydrolase ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo investigate the expression of ZBTB8A (zinc finger and BTB domain containing 8A) in gastric cancer tissues and its clinical significance.

METHODSLevel of ZBTB8A mRNA in human normal gastric cell line GES-1, human gastric cancer cell line SGC7901 and MGC803 was detected by real-time PCR. Levels of ZBTB8A mRNA and protein in cancer tissues, adjacent cancer tissues from 104 cases with primary gastric cancer and normal gastric mucosal tissues from 40 cases without malignant gastric diseases were detected by RT-PCR and immunohistochemistry, respectively. Association between ZBTB8A expression and clinicopathology was analyzed.

RESULTSZBTB8A mRNA expressions in SGC7901, MGC803 and GES-1 cells were 0.00138±0.00015, 0.00158±0.00021, 0.00036±0.000055, respectively, and differences among SGC7901, MGC803 and GES-1 were significant respectively (all P<0.05). ZBTB8A mRNA expression was significantly up-regulated in cancer tissues as compared to adjacent cancer tissues and normal tissues (0.0152±0.0126 vs. 0.0070±0.0061 and 0.0079±0.0036, all P>0.05), while no significant difference was found between adjacent cancer tissues and normal tissues (P>0.05). ZBTB8A expression was significantly associated with invasive depth, lymph node metastasis, tumor stage, and degree of adenocarcinoma differentiation (all P<0.05), but not with age, gender, histological type,gross type (all P>0.05).

CONCLUSIONZBTB8A may be a potential carcinogenic factor in gastric carcinoma, and may also be involved in gastric adenocarcinoma cell differentiation, cancer invasion and metastasis.

Adenocarcinoma ; metabolism ; Cell Line, Tumor ; Female ; Humans ; Kruppel-Like Transcription Factors ; metabolism ; Lymphatic Metastasis ; Male ; Middle Aged ; RNA, Messenger ; genetics ; Stomach Neoplasms ; metabolism

The aim of this study was to investigate the expression of Krupple-like factor 4 (KLF-4) in human umbilical vein endothelial cells (HUVEC) under stimulating of cytokines IL-1beta and TNF-alpha. The HUVEC were isolated, cultured and exposed to IL-1beta, TNF-alpha for 2 and 4 hours, the expression level of KLF-4 mRNA was detected by real-time PCR, the expression level of KLF-4 protein was measured by Western blot, the location of KLF-4 in HUVEC was determined by confocal laser microscopy. The results showed that the KLF-4 mRNA lowly expressed in normal HUVEC, but highly expressed in HUVEC after stimulation with IL-1beta and TNF-alpha; furthermore the expressions of KLF-4 mRNA and protein were enhanced along with prolonging of time. Confocal laser microscopy showed that the expression of KLF-4 was enhanced in nucleus and plasma of HUVEC after stimulating with IL-1beta. It is concluded that the expression of KLF-4 increases under IL-1beta and TNF-alpha stimulation which may participate in regulation of endothelial activity.
Cells, Cultured ; Endothelium ; metabolism ; Humans ; Interleukin-1beta ; pharmacology ; Kruppel-Like Transcription Factors ; metabolism ; RNA, Messenger ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology