Objective To identify the changes of DNA methylation profile in the process of malignant transformation of BEP2D cell induced by α particles.Methods The genomic DNAs were isolated from the malignant transformation BERP35T4 cells and immortalized human bronchial epithelial cell line BEP2D.Genomic DNAs were digested by MseI and ligated of PCR linkers.Methylated DNAs were digested by BstUI and amplified by PCR.The methylated DNA probes were prepared by labeling with Cy3 and Cy5 fluorescence dyes individually and hybridized to the methylation CpG-Island microarray.The hybridization results were scanned and analyzed.Intensity values were quality controlled and normalized.The normalized data were used to identify the differentially expressed genes based on a 1.5 fold difference of the expression level.Results There were 16 genes which showed changes of methylation level in malignant transformation BERP35T4 cells, 9 of them were hypermethylation and 7 were hypomethylation.These genes were including the SKIP gene, PPP3CC gene, MAP2K6 gene, KIR2DL1 gene, KIR2DL4 gene, KIR3DP1 gene, ZNF493 gene, ZNF100 gene, NKX2-5 gene, TFAP2D gene, DR1 gene, KCNJ16 gene, CCDC18 gene, FNBP1L gene, IRX4 gene, EPB41L3 gene, TCP10 gene and so on.Conclusions The DNA methylation might have effects on ionizing radiation drived tumorigenesis.

Objective To explore the effect of transcription factor FOXO3a on the signaling pathway of PTEN regulating the expression of RAD51.Methods Western blotting was used both to determine the phosphorylation of FOXO3a in both Pten+/+ and Pten-/-MEFs cells and to detect the phosphorylation of FOXO3a in Pten+/+ MEFs cells transfected with Flag-Akt WT or Flag-Akt AC(activated Akt),and Pten-/-MEFs cells transfected with Flag-PtEN WT or Flag-Akt DN(inactivated Akt).Results Higher phosphorylation of FOXO3a was found in Pten-/-MEFs cells compared to Pten+/+ MEFs cells,and the increased level of phosphorylated Akt was mainly found in the nuclei of Pten-/-MEFs cells.Transfection of exogenous Pten gene into Pten-/-MEFs resulted in a decreased phosphorylation of FOXO3a in the nucleus.In contrast,Pten+/+ MEFs transfected with exogenous akt gene showed a rising phosphorylation of FOXO3a in the nucleus.siRNA-mediated knockdown of FOXO3a gene resulted in a decreased expression of RAD51 protein in Pten+/+MEFs cells.Conclusion FOXO3a can bind to the transcriptional region of RAD51 gene,through which PTEN/ PI3K/Akt/FOXO3a signaling pathway regulates the expression of RAD51.

An increased level of spontaneous DNA double-strand breaks in Pten deficient cells was previously reported. Here we investigated whether and how the anti-oncogene pten may regulate the expression of rad51,a key component for homologous recombination in DNA double-strand break repairs.The rad51 mRNA level in the Pten -/- MEFs cells was down-regulated as shown by real-time PCR. After LY294002 (an antagonist of PTEN to inhibit PI3K) treatment,the RAD51 mRNA was increased. The transfection of Flag-Akt WT (Akt wild-type as the PI3K down-stream target) or Flag-AC (constitutively activated Akt) decreased the RAD51 at both mRNA and protein levels in Pten +/+ MEFs cells. In contrast,the Pten WT or Akt-DN (inactivated Akt) transfection augmented levels of rad51 expression as compared to the cells transfected with the control Flag-Vec vector. The siRNA-mediated suppression of akt resulted in an increased expression of RAD51 protein in pten -/- MEFs cells. The results suggested that PTEN positively regulated rad51 expression,and the PI3K /Akt signaling pathway might be involved.

BACKGROUND:In eukaryotic cells, there are two sub-pathways of nucleotide excision repair (NER), the global genome (gg) NER and the transcription-coupled repair (TCR). TCR can preferentially remove the bulky DNA lesions located at the transcribed strand of a transcriptional active gene more rapidly than those at the untranscribed strand or overall genomic DNA. This strand-specific repair in a suitable restriction fragment is usually determined by alkaline gel electrophoresis followed by Southern blotting transfer and hybridization with an indirect end-labeled single-stranded probe. Here we describe a new method of TCR assay based on strand-specific-PCR (SS-PCR). Using this method, we have investigated the role of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), a member of the phosphatidylinositol 3-kinase-related protein kinases (PIKK) family, in the TCR pathway of UV-induced DNA damage.RESULTS:Although depletion of DNA-PKcs sensitized HeLa cells to UV radiation, it did not affect the ggNER efficiency of UV-induced cyclobutane pyrimidine dimers (CPD) damage. We postulated that DNA-PKcs may involve in the TCR process. To test this hypothesis, we have firstly developed a novel method of TCR assay based on the strand-specific PCR technology with a set of smart primers, which allows the strand-specific amplification of a restricted gene fragment of UV radiation-damaged genomic DNA in mammalian cells. Using this new method, we confirmed that siRNA-mediated downregulation of Cockayne syndrome B resulted in a deficiency of TCR of the UV-damaged dihydrofolate reductase (DHFR) gene. In addition, DMSO-induced silencing of the c-myc gene led to a decreased TCR efficiency of UV radiation-damaged c-myc gene in HL60 cells. On the basis of the above methodology verification, we found that the depletion of DNA-PKcs mediated by siRNA significantly decreased the TCR capacity of repairing the UV-induced CPDs damage in DHFR gene in HeLa cells, indicating that DNA-PKcs may also be involved in the TCR pathway of DNA damage repair. By means of immunoprecipitation and MALDI-TOF-Mass spectrometric analysis, we have revealed the interaction of DNA-PKcs and cyclin T2, which is a subunit of the human transcription elongation factor (P-TEFb). While the P-TEFb complex can phosphorylate the serine 2 of the carboxyl-terminal domain (CTD) of RNA polymerase II and promote transcription elongation.CONCLUSION:A new method of TCR assay was developed based the strand-specific-PCR (SS-PCR). Our data suggest that DNA-PKcs plays a role in the TCR pathway of UV-damaged DNA. One possible mechanistic hypothesis is that DNA-PKcs may function through associating with CyclinT2/CDK9 (P-TEFb) to modulate the activity of RNA Pol II, which has already been identified as a key molecule recognizing and initializing TCR.

OBJECTIVE:To explore the effect of genomic stability of PTEN-deficient mice embryonic fibroblasts after transfection with RAD51,an important homologous recombination repair gene.METHODS: Immunofluorescence assay was used to observe the number of spontaneousγ-H2AX foci.Neutral single cell gel electrophoresis was applied to detect spontaneous and radiation-induced DNA double-strand breaks in both PTEN-deficient and PTEN wild-type cells.RESULTS:PTEN deletion led to an increase of spontaneousγ-H2AX foci and the length of tail moment,indicating DNA double-strand breaks.Transfection with RAD51 increased cell survival and decreased radiation-induced DNA double-strand breaks of PTEN-deficient cells.CONCLUSION:Homologous recombination gene RAD51 could increase genomic stability of PTEN-deficient cells.

Background When DNA double-strand breaks (DSB) are induced by ionizing radiation (IR) in cells, histone H2AX is quickly phosphorylated into γ-H2AX (p-S139) around the DSB site. The necessity of DNA-PKcs in regulating the phosphorylation of H2AX in response to DNA damage and cell cycle progression was investigated. Results The level of γH2AX in HeLa cells increased rapidly with a peak level at 0.25 - 1.0 h after 4 Gy γ irradiation. SiRNA-mediated depression of DNA-PKcs resulted in a strikingly decreased level of γH2AX. An increased γH2AX was also induced in the ATM deficient cell line AT5BIVA at 0.5 - 1.0 h after 4 Gy γ rays, and this IR-increased γH2AX in ATM deficient cells was dramatically abolished by the PIKK inhibitor wortmannin and the DNA-PKcs specific inhibitor NU7026. A high level of constitutive expression of γH2AX was observed in another ATM deficient cell line ATS4. The alteration of γH2AX level associated with cell cycle progression was also observed. HeLa cells with siRNA-depressed DNA-PKcs (HeLa-H1) or normal level DNA-PKcs (HeLa-NC) were synchronized at the G1 phase with the thymidine double-blocking method. At ~5 h after the synchronized cells were released from the G1 block, the S phase cells were dominant (80%) for both HeLa-H1 and HeLa-NC cells. At 8 - 9 h after the synchronized cells released from the G1 block, the proportion of G2/M population reached 56 - 60% for HeLa-NC cells, which was higher than that for HeLa H1 cells (33 - 40%). Consistently, the proportion of S phase for HeLa-NC cells decreased to ~15%; while a higher level (26 - 33%) was still maintained for the DNA-PKcs depleted HeLa-H1 cells during this period. In HeLa-NC cells, the γH2AX level increased gradually as the cells were released from the G1 block and entered the G2/M phase. However, this γH2AX alteration associated with cell cycle progressing was remarkably suppressed in the DNA-PKcs depleted HeLa-H1 cells, while wortmannin and NU7026 could also suppress this cell cycle related phosphorylation of H2AX. Furthermore, inhibition of GSK3β activity with LiCl or specific siRNA could up-regulate the γH2AX level and prolong the time of increased γH2AX to 10 h or more after 4 Gy. GSK3β is a negative regulation target of DNA-PKcs/Akt signaling via phosphorylation on Ser9, which leads to its inactivation. Depression of DNA-PKcs in HeLa cells leads to a decreased phosphorylation of Akt on Ser473 and its target GSK3β on Ser9, which, in other words, results in an increased activation of GSK3β. In addition, inhibition of PDK (another up-stream regulator of Akt/GSK3β) by siRNA can also decrease the induction of γH2AX in response to both DNA damage and cell cycle progression. Conclusion DNA-PKcs plays a dominant role in regulating the phosphorylation of H2AX in response to both DNA damage and cell cycle progression. It can directly phosphorylate H2AX independent of ATM and indirectly modulate the phosphorylation level of γH2AX via the Akt/GSK3 β signal pathway.

Objective To investigate the effect of Pten gene knock-out on expression of Rad51 gene and the potential mecha-nism of the effect.Methods The mRNA transcription levels of Rad51 gene related to repair by homologous recombination in Pten~(+/+)MEFs and Pten~(-/-)MEFs,the radiosensitivities of the two kinds of MEFs,as well as Rad51 mRNA transcription levels in the two kinds of MEFs after radiation,were compared by semi-quantitative RT-PeR and clone formation assay,and the potential mechanism was in-vesfigated.Results The Rad51 mRNA transcription level in Pten~(-/-)MEFs was significantly lower than that in Pten~(+/+)MEFs.Com-pared with that of Pten~(+/+)MEFs.the mdiosensitivity of Pten~(-/-)MEFs also decreased significantly.However,both the Rad51 mRNAtranscription levels in Pten~(-/-)MEFs after radiation and after treatment with LY-294002,an inhibitor of PI 3K/AKT signal pathway,in-creased significantly.Conclusion Abnormal expression of Rad51 gene WaS observed after knock-out of Pten gene.Pten might regu-late the expression of Rad51 gene through P13K/AKT signal pathway.

目的 研究Pten基因对抗氧化蛋白Cu/Zn-SOD基因表达的调控,初步探索其调控机制.方法 运用Northern blot比较Pten+/-MEFs与Pten-/-MEFs细胞中基础Cu/Zn-SOD mRNA表达差异,以及0.1 mmol/L H2O2诱导后Pten+/-MEFs与Pten-/-MEFs细胞中Cu/Zn-SOD mRNA表达差异;运用Western blot分析P13K/AKT通路抑制剂LY294002作用Pten-/-MEFs细胞不同时间(30 min,1、2、6、24 h)后,与空白Pten-/-MEFs细胞相比,磷酸化AKT及Cu/Zn-SOD蛋白表达变化;利用Northern blot分析LY294002作用Pten-/-MEFs细胞30 min,1、2、6、24 h后,与空白Pten-/-MEFs细胞相比,Cu/Zn-SOD mRNA表达变化.结果 Pten-/-MEFs细胞中,基础Cu/Zn-SOD mRNA表达水平降低,H2O2诱导的Cu/Zn-SOD mRNA表达明显受到抑制;在LY294002作用Pten-/-MEFs细胞30 min时,AKT磷酸化水平明显降低,2 h时基本没有表达;与此对应,在LY294002作用Pten-/-MEFs细胞30 min时,Cu/Zn-SOD蛋白及mRNA表达均增强,并持续增强至24 h.结论 小鼠胚胎成纤维细胞中,Pten基因可通过拮抗PI3K/AKT信号通路调控Cu/Zn-SOD蛋白及mRNA的表达.

Despite the significance of cigarette smoke for carcinogenesis, the molecular mechanisms that lead to increased susceptibility of human cancers are not well-understood. In our present study, the oncogenic transforming effects of cigarette smoke condensate (CSC) were examined using papillomavirus-immortalized human bronchial epithelial cells (BEP2D). Growth kinetics, saturation density, resistance to serum-induced terminal differentiation, anchorage-independent growth and tumorigenicity in nude mice were used to investigate the various stages of transformation in BEP2D cells. Illumina microarray platforms were used to explore the CSC-induced alteration of global mRNA expression profiles of the earlier period and the advanced stage of CSC-treated BEP2D cells. We showed here that a series of sequential steps arose among CSC-treated immortalized human bronchial epithelial cells, including altered growth kinetics, resistance to serum-induced terminal differentiation, and anchorage-independence growth. In the earlier period of CSC treatment, 265 genes were down-regulated and 63 genes were up-regulated, respectively, and in the advanced stage of CSC treatment, 313 genes were down-regulated and 145 genes were up-regulated, respectively. Notably, among those genes, the expression of some of imprinted genes such as IGF2, NDN, H19 and MEG3 were all silenced or down-regulated in CSC-treated cells. These genes reactivated after 5μM 5-aza-2-deoxycytidine (5-aza-dC) treatment. These results demonstrated that long-term treatment of human bronchial epithelial cells with CSC may adversely affect their genetic and epigenetic integrity and lead to further transformation.

Objective: To analyze the effect of interleukin-1 involved in expression regulation of Schlafen2(Slfn2) in the pleiotrophin(Ptn) knock down mouse embryo fibroblast cell lines.Methods: In the previous study,we found the mRNA expression of Slfn2 gene and interleukin-1(IL-1) was increased in Ptn-siRNA B/MEF241 cells when compared to control cells.In this study,mRNA expression of Slfn2 gene was detected in the control cells that incubated with the supernatant of Ptn-siRNA B/MEF241 cells.Then the expression change of IL-1α and IL-1f6 was detected in the Ptn-siRNA B/MEF241 cells treated by 50 ng/μl recombinant human PTN(rh PTN).We investigated the induction of Slfn2 gene expression in the presence of rhIL-1ra and IL-1α affinity purified polyclonal antibody.Results:(1)The expression of Slfn2 in the control cells can be induced by incubation with the culture medium of Ptn-siRNA B/MEF241 cells.(2)Using rh PTN can inhibit the expression of IL-1α and IL-1f6 in Ptn-siRNA B/MEF241 cells.(3)The expression of Slfn2 in the Ptn-siRNA B/MEF241 cells can be inhibited in the presence of rhIL-1ra and IL-1α affinity purified polyclonal antibody.Conclusion: IL-1 may play an important role in pleiotrophin negative regulation of Slfn2 in Ptn-siRNA B/MEF241 cells.

Objective: To investigate the transcription regulation of matrix metalloproteinase (MMP) 3,10 by pleiotrophin (PTN).Methods: The mRNA expression levels of MMP3,MMP10 were compared between control and PTN knocking down MEF cells by RT-PCR and Northern Blot.Then,50 ng/mL PTN was added in culture medium of the PTN knocking down MEF cells to investigate the effect of pleiotrophin on the transcription of MMP3,MMP10.Results: MMP3,MMP10 expressed higher in the cell that PTN was absence,but they expressed lower after the PTN effected.Conclusion:PTN negative regulated the expression of MMP3 and MMP10.

Objective:To study protein variation between Pten+/+MEFs and Pten-/-MEFs cells. Methods:Two dimensional electrophoresis was employed to compare the differential expression proteins between Pten+/+MEFs and Pten-/-MEFs cells. The differential expression proteins were digested in gel by enzyme and the mass of generated peptides were measured by matrix assisted laser desorption ionization time of flight mass spectrometry. The data obtained from peptide mass fingerprinting was searched using the internet available database. The expressions of some identified proteins were confirmed using Northern blot and Western blot. Results:The Cu/Zn-SOD,Prx5 and Prx6 were down-regulated while the cofilin 1 and low molecular weight protein tyrosine phosphatase were up-regulated in Pten-/-MEFs cells. The expression of Cu/Zn-SOD,Prx5 and Prx6 was confirmed using Northern blot and Western blot. Conclusion:The protein profile of Pten-/-MEFs cell lines displayed obviously difference compared to that of Pten+/+MEFs cell lines. The results implied that various distinct different proteins might lead to cancer.

目的 研究H2O2、PTEN与肽类生长因子(胰岛素等)在调控Akt激酶活性中的作用及其相互关系.方法 Western Blot检测对照小鼠胚胎成纤维细胞PTEN MEFs和PTEN基因敲除小鼠胚胎成纤维细胞PTEN MEFs中PTEN蛋白表达的差异.用胰岛素及NADPH氧化酶(NOX)抑制剂--DPI作用PTEN MEFs和PTEN MEFs细胞,Western Blot检测Akt激酶蛋白磷酸化水平的变化.将细胞接种于96孔板,加入胰岛素及DPI,96h后MTT法检测细胞增殖的变化.结果 在对照PTEN MEFs细胞内,加入胰岛素(100mU/ml)15min后Akt激酶磷酸化水平明显上调,加入10μmol/L DPI处理30min后,Akt激酶磷酸化恢复到基础水平,在PTEN MEFs细胞中未观察到上述变化.经胰岛素作用后PTEN MEFs细胞增殖加快(P＜0.05),加入DPI作用后可减缓细胞的增殖(P＜0.05),胰岛素和DPI同时作用对其增殖无明显影响(P＞0.05);各种处理因素对PTEN MEFs细胞增殖均无明显影响(P均＞0.05).结论 肽类生长因子可以通过磷酸化激活Akt激酶,这一过程依赖于H2O2的产生和抑癌基因PTEN的存在.

Objective:To establish cell lines which can stably express Schlafen2(Slfn2)gene and to elucidate biological functions of the gene.Methods:pEGFP-Slfn2 eukaryotic expressing vector was constructed. Control and pEGFP-Slfn2 vectos were transiently transfected into NIH/3T3 cells to observe the distribution of Slfn2 protein directly by laser scanning confocal microscopy. Control and pEGFP-Slfn2 were stably transfected into NIH/3T3 cells and G418 screening was used to obtain resistant cell strains. The expression of Slfn2 was measured by Northern blot.The growth curve and Transwell were used to analyze the effects of Slfn2 on cell proliferation and migration. Results:By establishing cell lines which could express Slfn2 stably,it was shown that the proteins expressed by the gene were detected in cell nucleus and cytoplasm. Proliferation and migration were inhibited markedly when Slfn2 was overexpressed in these cells.Conclusions: The results suggest that Slfn2 is a potential tumor suppressor gene.

On 25 June 1990, a radiation accident occurred in a 60Co source radiation unit in Shanghai, due to violations in operation regulations. This accident resulted in the exposure of seven individuals to acute high-dose and dose-rate whole-body external irradiation. Conventional chromosomal aberration analysis, G-banding automatic karyotype analysis and/or fluorescent in situ hybridization (FISH) painting methods were used to analyze chromosomal aberrations in peripheral blood lymphocytes from five of the victims 24 h to 17 years after accidental exposure to 1.9–5.1 Gy of 60Co γ-rays. The frequency of unstable chromosomal aberrations (dicentrics and rings) remained at constant levels 1 month after exposure. Three months after exposure, the frequency was reduced by 20–40% in three victims, while no reduction was seen in the other two victims. Twelve years after exposure, the number of dicentrics and rings decreased by more than 90%, and did not reveal a dose-dependent relationship. However, even at 12–17 years after exposure, stable chromosome aberrations, dominated by translocations, remained at a high level in a dose-dependent manner. The frequency of stable chromosomal aberrations detected by FISH showed a similar dose-dependent relationship as that detected by karyotype analysis of G-banding chromosomes. The G-banding analysis also suggested that the pattern of chromosome breakpoints is random. The FISH data showed a decreasing tendency with time for chromosome translocation frequency in the peripheral lymphocytes, and the rate of reduction varied among different individuals. It is likely that the higher dose the victim received, the lesser the translocation frequency decreased with time. The G-banding data also showed that the rate of reduction of translocations is different among individuals. From 5 to 17 years after accidental irradiation, a very small reduction (~10%) of translocation frequency was observed in victims C and D, while there was about a 35% reduction (the highest among the victims) for victim G who received the smallest dose (1.9 Gy). These observations can be used to validate the existence of chromosomal aberrations in peripheral blood lymphocytes as a biological dosimeter for radiation exposures.

Objective: To study protein variation between PtenL/L MEFs and Pten Δ/Δ MEFs cells. Methods: Two-dimensional electrophoresis (2-DE) was employed to compare the differential expression proteins between PtenL/L MEFs and PtenΔ/Δ MEFs cells. Six differential expression proteins were digested in gel by enzyme and the mass of generated peptides was measured by matrix assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). The data obtained from peptide mass fingerprinting (PMF) were searched using the Internet available database and five proteins were identified. Results: Compared with that of PrenL/L MEFs, expression level of proteins including phosphoglycerate mutase 1 (PGAM1) and peptidyl-prolyl cis-trans isomerase C (PPIC) was up-regulated, whereas expression level of Transgelin 2 was down-regulated in PtenΔ/Δ MEFs cells. B and F proteins were both identified to be peroxiredoxin-6. They had similar molecular weight but different PI which might be caused by post-translation modification. B protein was only expressed in PtenΔ/Δ MEFs cells. Conclusion: The protein profile of PtenΔ/Δ MEFs cells displayed obvious difference compared to that of PtenL/L MEFs cells. The results implied that various distinct different proteins might lead to cancer.

BACKGROUND AND AIM:In 1990,2 severe and 3 moderate degree acute radiation syndrome(ARS) victims in Shanghai 6.25 60Co accident were cured.To investigate late effects of ARS,14 years continuous follow-up study of chromosomal aberrations in these 5 victims was performed to accumulate valuable data on late effect of radiation.MATERIALS AND METHODS:Conventional chromosome aberration,G-banding automatic karyotype analysis and whole chromosome probe painting FISH technique were used simultaneously to examine unstable and stable chromosome aberrations and compare the results over 14 years.RESULTS:Unstable aberrations declined to approximately 20% of initial level 3.5 years after exposure and was totally lost after 14 years.Stable aberrations such as reciprocal translocations were found predominantly.The results of G-banding karyotype analysis and FISH were very similar.The frequencies of Cs and complicated aberrations showed a dose-response relationship and remained at a relatively stable level 6-14 years after exposure.The break frequencies of each chromosome distributed randomly.The recovery speed of chromosome aberrations and degree of late effect related not only to exposure dose but also to the victims' health condition.CONCLUSION:Stable chromosome aberrations were fairly ideal in the assessment of radiation late effects.It is important to make long-term follow-up study for the victims exposed to accidental irradiation.

It is recently reported that tumor suppressor pten,encoding a protein and lipid phosphatase,plays a critical role in maintaining chromosomal integrity and genetic stability through phosphatase-dependent pathway as well as phosphatase-independent pathway.The mechanism of phosphatase-dependent pathway works mainly via PI3K/AKT way and the mechanism of phosphatase-independent pathway is mainly via interaction between proteins.In addition,there are still some pathways which have not been identified.

Objective: To investigate the mechanisms of interleukin-1(IL-1) involved in expression regulation of Schlafen2 (Slfn2) in the pleiotrophin(Ptn) knock down mouse embryo fibroblast cells line. Methods: The effect of cell density of PtnsiRNA B / MEF241 cells on Slfn2 expression was examined through Northern blot. Different concentration of IL-1α affinity purified polyclonal antibody and rhIL-1ra were used to incubate Ptn-siRNA B / MEF241 cells and the expression of Slfn2 gene was investigated. Different concentration of IL-1α antibody and rhIL-1ra were used to incubate Ptn-siRNA B / MEF241 cells and the phosphorylation level of JNK was examined through Western blot. The effect of SP600125(JNK / MAPK inhibitor) on transcription of Slfn2 in Ptn-siRNA B / MEF241 cells was investigated through Northern blot. Results: Slfn2 expression was subject to cell density control. Interruption of IL-1 could suppress Slfn2 gene expression. Suppression of IL-1 could affect activation of JNK. Interruption of JNK could suppress Slfn2 gene expression. Conclusion: The expression of Slfn2 was regulated by IL-1 through the JNK / MAPK pathway in Ptn-siRNA B / MEF241 cells.