Silencing KLF16 inhibits oral squamous cell carcinoma cell proliferation by arresting the cell cycle and inducing apoptosis

Krüppel-like factor 16 (KLF16), a member of the Krüppel-like factor (KLF) family, has been extensively investigated in multiple cancer types. However, the role of KLF16 in oral squamous cell carcinoma (OSCC) remains unknown. Thus, we conducted this study to investigate its related mechanism. KLF16 expression in OSCC cell lines was quantified by western blotting. Then, OECM1 and OC3 cells were divided into Blank, siCtrl, siKLF16#1 and siKLF16#2 groups. Subsequently, cell proliferation was detected using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assays, cell migration and invasion were detected with wound healing and Transwell assays, and cell cycle distribution and cell apoptosis were detected via flow cytometry. KLF16, p21, CDK4, Cyclin D1 and p-Rb expression was detected by western blotting. Finally, xenograft models were established in nude mice to observe the in vivo effects of KLF16 on OSCC. KLF16 protein expression was upregulated in OSCC cells. Compared to the cells in the Blank group, the OECM1 and OC3 cells in the siKLF16#1 group and siKLF16#2 group exhibited a sharp decrease in proliferation but a remarkable increase in apoptosis. Moreover, the proportion of cells in the G0/G1 phase notably increased and that in the S phase decreased, with evident decreases in cell invasion and migration. Moreover, KLF16, cyclin-dependent kinase 4 (CDK4), Cyclin D1 and p-Rb protein expression was upregulated, but p21 expression was downregulated. The mice in the siKLF16#1 and siKLF16#2 xenograft model groups exhibited slower tumour growth and smaller tumours with evident downregulation of Ki67 expression compared to the mice in the Blank group. KLF16 expression was upregulated in OSCC cells, and interfering with KLF16 led to cell cycle arrest, inhibited OSCC cell growth and promoted cell apoptosis.     

Zebrafish KLF4 is essential for anterior mesendoderm/pre-polster differentiation and hatching.

Gene knockout studies of Krüppel-like factors (KLFs) in mice have shown essential roles in organogenesis. A screen for KLF family members in zebrafish identified many KLFs. One of these, zebrafish KLF4 (zKLF4) is the homologue of neptune, a Xenopus laevis KLF. zKLF4 is expressed from approximately 80% epiboly a patch of dorsal/anterior mesendodermal cells called the pre-polster and, subsequently, in the polster and hatching gland. Here we investigate the function of zKLF4 using morpholino-based antisense oligonucleotides. Knockdown of zKLF4 resulted in complete absence of hatching gland formation and subsequent hatching in zebrafish. In addition, there was early knockdown of expression of the pre-polster/anterior mesendoderm markers CatL, cap1, and BMP4. These results indicate zKLF4 is expressed within the pre-polster, an early mesendodermal site, and that it plays a critical role in the differentiation of these cells into hatching gland cells.     

Krüppel-like factor 2 controls IgA plasma cell compartmentalization and IgA responses

Krüppel-like factor 2 (KLF2) is a potent regulator of lymphocyte differentiation, activation and migration. However, its functional role in adaptive and humoral immunity remains elusive. Therefore, by using mice with a B cell-specific deletion of KLF2, we investigated plasma cell differentiation and antibody responses. We revealed that the deletion of KLF2 resulted in perturbed IgA plasma cell compartmentalization, characterized by the absence of IgA plasma cells in the bone marrow, their reductions in the spleen, the blood and the lamina propria of the colon and the small intestine, concomitant with their accumulation and retention in mesenteric lymph nodes and Peyer's patches. Most intriguingly, secretory IgA in the intestinal lumen was almost absent, dimeric serum IgA was drastically reduced and antigen-specific IgA responses to soluble Salmonella flagellin were blunted in KLF2-deficient mice. Perturbance of IgA plasma cell localization was caused by deregulation of CCR9, Integrin chains αM, α4, β7, and sphingosine-1-phosphate receptors. Hence, KLF2 not only orchestrates the localization of IgA plasma cells by fine-tuning chemokine receptors and adhesion molecules but also controls IgA responses to Salmonella flagellin.     

Krüppel样因子4在肿瘤发生、发展中的作用

Krüppel样因子4(Krüppel-like factor 4,KLF4)是含有3个锌指结构的转录因子,在细胞微环境中参与不同的细胞信号网络,调控靶基因的转录活化或抑制,与细胞的增殖分化、诱导型多能干细胞的生成有关,具有癌基因和抑癌基因、促炎和抗炎等双向调节功能.KLF4的表达与肿瘤的预后相关,可作为肿瘤靶向治疗的...     

Krüppel样因子4在猪脂肪间充质干细胞成脂分化过程中的表达模式

目的探讨猪脂肪间充质干细胞(AMSCs)成脂分化过程中Krüppel样因子4(KLF4)的表达模式。方法采用F3代以上猪AMSCs进行成脂诱导分化,用油红O染色提取法检测成脂分化程度,用RT-PCR和Realtime PCR检测KLF4的表达模式。结果猪AMSCs成脂诱导分化,诱导3 d开始出现脂肪滴,诱导10 d时成脂分化率达60%;RT-PCR检测,在诱导分化2、4、8、12和16 d时都能检测出KLF4的表达;经Real-time PCR检测,上述各诱导分化时间点的表达量分别为对照组的1.6657±0.2269、2.6790±0.0524、2.6293±0.0280、2.3633±0.1568和2.6146±0.1575倍。这些结果表明,KLF4的表达在猪AMSCs成脂诱导分化的第2天就有显著上调,表达高峰出现在成脂分化的第4天,此后持续高表达。结论在猪AMSCs成脂分化过程中,从早期到晚期,KLF4发挥持续性的调控作用。