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BackgroundPulmonary sarcomatoid carcinoma (PSC) is a rare and aggressive disease without standardized treatment strategies. The efficacy of second-line or beyond immune checkpoint inhibitors (ICIs) has been proven in recent studies, whereas the evidence for first-line immunotherapy for PSC is still limited to case reports and remains poorly understood.Materials and methodsThis was a multicenter, retrospective analysis of 21 patients with a histological diagnosis of PSC who received ICI as first-line therapy from January 2019 to March 2022. The expression of PD-L1 was evaluated by immunohistochemistry (IHC) using the monoclonal antibody 22C3. Low and high PD-L1 expressions were defined using the tumor proportion score (TPS), with cutoffs of 1 and 50%, respectively.ResultsAll eight patients had PD-L1 positivity who underwent PD-L1 expression assessment, and six patients (6/8, 75.0%) had high PD-L1 expression. Among the 21 PSC patients, seven received tislelizumab, six received camrelizumab, four received sintilimab, three received pembrolizumab, and one received durvalumab. Among them, 18 PSCs received combination therapy, whereas another three PSCs received immunotherapy alone. Out of the 21 PSC patients, 12 (57.1%) achieved a partial response (PR), and five patients had stable disease (SD) as the best response, whereas four PSCs experienced dramatic progressive disease (PD). The median progression-free survival (PFS) was 9.2 (95% CI [4.3, 14.1]) months, and the median OS was 22.8 (95% CI [4.0, 41.5]) months. Among the three treatment groups (immunotherapy alone, immunotherapy combined with anlotinib, and chemoimmunotherapy), the median PFS was 8.0, 9.4, and 9.6 months, and the median OS was 19.0, 22.8, and 30.6 months, respectively. There was no difference in PFS and OS between the three treatment regimen groups (P = 0.86 and P = 0.34, respectively) and different immunotherapies (P = 0.10 and P = 0.23, respectively). No serious adverse events (grade ≥ 3) were noted.ConclusionFirst-line immunotherapy has promising therapeutic potential in the treatment of PSC. More studies are warranted to confirm these findings.

ETS-related gene (ERG) is the member of ETS-family of transcription factors and is commonly expressed in Ewing sarcoma. Recently, we found that ERG can also be expressed in lymphoblastic lymphoma. The aim of this article is to explore the expression patterns of ERG in T-lymphoblastic lymphoma, and to evaluate its diagnostic value for differentiating T-lymphoblastic lymphoma and nonneoplastic T-precursor cells in thymoma via immunohistochemistry. In this study, we explored the expression pattern of ERG in T-lymphoblastic lymphoma and thymoma specimens via immunohistochemistry. Sixteen T-lymphoblastic lymphoma and 18 thymoma specimens were evaluated for the expression of ERG. Our findings showed that ERG was expressed in 10 of the 16 (63%) T-lymphoblastic lymphoma specimens, and in only 1 of the 18 (6%) thymoma specimens. The positive and negative predictive value of ERG in T-lymphoblastic lymphoma was 91% and 74%, respectively. ERG is a helpful marker for the diagnosis of T-lymphoblastic lymphoma and is a promising new method to differentiate T-lymphoblastic lymphoma and the nonneoplastic T-precursor cells in thymoma.

Most endoscopists routinely perform moderate or deep sedation for esophagogastroduodenoscopy (EGD). Considering that there is no consensus on the optimal sedation depth and it varies from country to country, our study aims to compare the effectiveness, cost and safety of these two sedation methods in the Chinese population.This quasi-experimental study included a total of 556 eligible patients from July 2020 to June 2021, and they entered the moderate sedation group or deep sedation group based on their choices. Baseline information, scores of Patient Satisfaction with Sedation Instrument (PSSI) and Clinician Satisfaction with Sedation Instrument (CSSI), examination time, sedation time, recovery time, expenses before medicare reimbursement, hypoxaemia and hypotension were compared between the two groups. Propensity Score Matching (PSM) analysis was conducted to balance the confounding factors.After PSM, 470 patients were involved in the analysis, with 235 for each group. The moderate sedation was clearly superior to the deep sedation group in terms of PSSI score (98.00 ± 0.94 vs. 97.29 ± 1.26), CSSI score (98.00 ± 0.78 vs. 97.67 ± 1.30), sedation time (11.90 ± 2.04 min vs. 13.21 ± 2.75 min), recovery time (25.40 ± 3.77 min vs. 28.0 ± 4.85 min), expenses (433.04 ± 0.00 Yuan vs. 789.85 ± 0.21 Yuan), with allModerate sedation presented better effectiveness and safety and lower cost, and thereby it should be recommended as a widely used sedation method in clinical practice in China.

Background Jumonji AT-rich interactive domain 1B(JARID1B) has been shown to be upregulated in many human cancers and plays a critical role in the development of cancers cells. Nevertheless, its functional role in colorectal cancer (CRC) progression is not fully understood. Methods Herein, JARID1B expression levels were detected in clinical CRC samples by western blotting and qRT-PCR. DLD-1 cells with JARID1B knockdown or overexpression by stably transfected plasmids were used in vitro and in vivo study. Colony formation, 5-ethynyl-20-deoxyuridine (EdU) and Real Time Cellular Analysis (RTCA) assays were used to detect cell proliferation and growth. Transcriptome and CHIP assays were used to examine the molecular biology changes and molecular interaction in these cells. Nude mice was utilized to study the correlation of JARID1B and tumor growth in vivo. Results Here, we first observed that JARID1B was significantly upregulated in CRC tissue compared to adjacent normal tissues. In CRC patients, JARID1B high expression was positively relation with poor overall survival. Multivariate analyses revealed that high JARID1B expression was an independent predictive marker for the poor prognosis of CRC. In addition, we found that JARID1B promoted CRC cells proliferation by Wnt/β-catenin signaling pathway. Further studies demonstrated CDX2 as a downstream target of JARID1B, and our data demonstrated that CDX2 is crucial for JARID1B -mediated Wnt/β-catenin signaling pathway. Mechanistically, we demonstrated that JARID1B regulated CDX2 expression through demethylation of H3K4me3. Conclusions CDX2 inhibited by JARID1B-derived H3K4me3 methylation promoted cells proliferation of CRC via Wnt/β-catenin signaling pathway. Therefore, our studies provided a novel insight into the role of JARID1B in CRC cells proliferation and potential new molecular target for treating CRC. Graphical abstract

BackgroundMelan-A/MART-1 is a melanocytic differentiation marker, which is recognized as an antigen on melanoma cells. It is relevant for pathologists as a useful diagnostic marker in the diagnosis of melanocytic tumors. However, the expressional pattern of Melan-A in poorly differentiated carcinoma of lung has never been reported so far.Case presentationHere, we report a 77-year-old female patient who presented with a large mass in the right lung and was subsequently diagnosed with a poorly differentiated carcinoma of lung. We unexpectedly found that the carcinoma in this patient exhibited diffuse Melan-A expression. ConclusionThis is the first case reported of a poorly differentiated carcinoma of lung with Melan-A expression. This report shows that Melan-A can express in poorly differentiated carcinoma, and highlights a potential diagnostic pitfall in the diagnosis of carcinoma, which urges pathologists to exercise caution in cases where Melan-A positivity and illustrates the need for further immunohistochemical or molecular examination to avoid misdiagnosis.

Background: The Ets-related gene (ERG) is the member of ETS family of transcription factors, which commonly expressed in Ewing's sarcoma. Recently, we found that ERG can also express in lymphoblastic lymphoma. The aim of this article is to analyze the ERG expression in lymphoblastic lymphoma. Methods: The patients of lymphoblastic lymphomas who had undergone fine needle aspiration or surgical operation from 2017 to 2021 in the second affiliated hospital of Nan-Chang university were collected and examined. Immunohistochemistry (IHC) was performed to evaluate the expression of ERG. Results: In this study, 20 T-lymphoblastic lymphomas and 4 B-lymphoblastic lymphomas were investigated for the expression of ERG. Our findings showed that ERG was expressed in 8 of the 20 (40%) T-lymphoblastic lymphomas, and 3 of the 4 (75.0%) B-lymphoblastic lymphomas. Conclusions: This report shows that ERG can express in lymphoblastic lymphomas, and highlights a potential diagnostic pitfall in the diagnosis of Ewing sarcoma, which urges pathologists to exercise caution in cases where ERG-positivity and illustrates the need for further immunohistochemical examination to avoid misdiagnosis.

Ubiquitin-specific protease 7 (USP7/HAUSP) is known to regulate multiple cellular phenomena, including cell cycle progression and proliferation, and is involved in binding and stabilizing specific target proteins through deubiquitylation. However, the detailed role of USP7 in papillary thyroid carcinoma (PTC) remains to be investigated. In this study, our results showed that USP7 was upregulated in PTC tissues compared with adjacent nontumour tissues. Consistently, a series of gain/loss functional assays in vivo and in vitro demonstrated the role of USP7 in promoting PTC cell proliferation. Furthermore, we showed that there was a negative correlation between USP7 and the CDK inhibitor p57

Glutamine metabolism plays an important role in cancer development and progression. Glutaminase C (GAC), the first enzyme in glutaminolysis, has emerged as an important target for cancer therapy and many studies have focused on the mechanism of enhanced GAC expression in cancer cells. However, little is known about the post-translational modification of GAC. Here, we report that phosphorylation is a crucial post-translational modification of GAC, which is responsible for the higher glutaminase activity in lung tumor tissues and cancer cells. We identify the key Ser314 phosphorylation site on GAC that is regulated by the NF-κB-PKCε axis. Blocking Ser314 phosphorylation by the S314A mutation in lung cancer cells inhibits the glutaminase activity, triggers genetic reprogramming, and alleviates tumor malignancy. Furthermore, we find that a high level of GAC phosphorylation correlates with poor survival rate of lung cancer patients. These findings highlight a previously unappreciated mechanism for activation of GAC by phosphorylation and demonstrate that targeting glutaminase activity can inhibit oncogenic transformation.

The aim of the present study was to analyze the association between the transcription factor forkhead box P3 (FOXP3) and diffuse large B-cell lymphoma (DLBCL), and investigate the effect of microRNA-155 (miR-155) on the generation and development of FOXP3 in DLBCL. The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) technique was used to determine the expression of FOXP3 in the human DLBCL cell lines Ly1, Ly8 and Ly10, and in normal B cells. An immunohistochemical method was used to determine FOXP3 expression in 60 DLBCL tumor and adjacent tissues, and a retrospective analysis of FOXP3 expression in tumor tissues and clinical data was performed. The lentiviral transfection technique was used to silence the miR-155 gene in mouse A20 cells to analyze the influence of miR-155 on FOXP3 in DLBCL. The A20 cell line with a silenced miR-155 gene was used to perform a tumorigenicity assay in BALB/c mice, and to compare the tumorigenicity rate and the tumor growth rate. The results identified that the expression of the transcription factor FOXP3 in the human DLBCL cell lines was increased compared with normal B cells; FOXP3 in human DLBCL tumor issues was increased compared with the tumor-adjacent tissue, and the increased expression of FOXP3 was identified as an indicator of poor prognosis of patients with DLBCL in the middle and late period; FOXP3 level decreased subsequent to silencing miR-155 in A20 cells; A20 cells with the low-expression miR-155 gene were used to determine the tumorigenicity in BALB/c mice and it was identified that the tumorigenicity of the low-expression miR-155 gene group was decreased compared with the untransfected group. Therefore, miR-155 may be a regulatory factor of FOXP3, and miR-155 may be associated with the metastasis and prognosis of patients with DLBCL.

Ubiquitin-specific protease 7 (USP7/HAUSP) is known to regulate multiple cellular phenomena, including cell cycle progression and proliferation, and is involved in binding and stabilizing specific target proteins through deubiquitylation. However, the detailed role of USP7 in papillary thyroid carcinoma (PTC) remains to be investigated. In this study, our results showed that USP7 was upregulated in PTC tissues compared with adjacent nontumour tissues. Consistently, a series of gain/loss functional assays in vivo and in vitro demonstrated the role of USP7 in promoting PTC cell proliferation. Furthermore, we showed that there was a negative correlation between USP7 and the CDK inhibitor p57KIP2 expression in PTC tissues and that USP7 facilitated PTC cell proliferation by inhibiting p57KIP2. Mechanistically, USP7 inhibited p57KIP2 expression by modulating TBX3, directly binding to TBX3, and decreasing its ubiquitination and degradation. Our findings demonstrated that USP7 played a critical oncogenic role in PTC tumorigenesis, suggesting that USP7 might act as a prognostic and therapeutic target for PTC progression.

Purpose Accumulating evidence indicates that long noncoding RNAs (lncRNAs) are aberrantly expressed in many cancer types, including hepatocellular carcinoma (HCC). lncRNA MYC-induced long non-coding RNA (MINCR) were revealed to be markedly up-regulated in gallbladder cancer and Burkitt lymphoma cells. However, the biological role and function of MINCR in HCC progression are still unknown. Methods The expression of MINCR in HCC tissues and cell lines was determined using quantitative real-time polymerase chain reaction assays. The effects of MINCR in HCC cell proliferation, migration, and invasion were determined using cell-counting kit 8 (CCK8) assay, wound healing assay, and Transwell assays in vitro. Results MINCR expression was up-regulated in HCC tissues and cell lines as compared with that in the negative control. The decreased expression of MINCR in vitro markedly inhibited HCC cell proliferation, migration, and invasion. Our results showed that MINCR is important in HCC development and may act as a therapeutic target that regulates HCC cellular proliferation, migration, and invasion, which are involved in HCC tumorigenesis. Conclusions To the best of our know ledge, MINCR in HCC has not been studied. Our findings showed that this study is the first to reveal that MINCR may act as a therapeutic target in HCC. The in-depth exploration of the molecular mechanism is required to illuminate the molecular mechanisms of MINCR in HCC development.

Micro (mi)RNAs are an endogenous non-coding small RNA comprised of 19-26 nucleotides. miRNAs regulate gene expression through the recognition of its 'seed sequence' and interactions with 3'-untranslated region of target miRNAs. Previous studies identified that miRNAs are associated with the onset and development of breast cancer and that a number of mutations in the coding DNA sequence of miRNAs affect its expression. Therefore, the present study aimed to screen differentially expressed miRNAs using miRNA expression profile chips to analyze the expression of miRNA (miR)-205 in 12 breast cell lines of different metastatic performance and benign proliferative variation as well as breast cancer via in-situ hybridization, and screen out single-nucleotide polymorphisms (SNPs) in the miR-205 coding gene region. In addition, the association between SNP and the clinicopathological features of breast lesions was investigated. The results of the present study demonstrated that the expression of miR-205 was decreased in breast cancer cells and tissues compared with benign lesions. SNPs in the miR-205 coding gene region were identified in tumor cell lines and as increasing lengths of the AGC repetitive sequence were lost, miR-205 expression increased. An association was identified between a number of SNPs in the miR-205 coding gene region and breast cancer, as well as between SNPs in miR-205 coding gene region and the clinicopathological features of breast cancer.

To aim of the present study was to investigate the association between special AT-rich DNA-binding protein-1 (SATB1) expression and liver cancer metastasis. SATB1 mRNA and protein expression in hepatocellular carcinoma tissues was analyzed by immunohistochemistry, and in two hepatocellular cancer cell lines, MHCC-97H (high metastatic potential) and HepG2 (low metastatic potential), by reverse transcription-polymerase chain reaction and western blot analysis. Transwell migration and wound-healing assays were also performed to investigate the metastasis of liver cancer following upregulation or silencing of SATB1 expression. The results revealed that SATB1 expression was significantly higher in hepatocellular carcinoma tissues compared with carcinoma-adjacent tissues. Furthermore, SATB1 expression was correlated with tumor size, differentiation degree, hemorrhage and/or necrosis, invasion and/or metastases and TNM stage. Both the mRNA and protein expression of SATB1 was higher in MHCC-97H cells than HepG2 cells. In addition, the migration capability of MHCC-97H cells was decreased after SATB1 silencing, whereas the migration capability of HepG2 cells was increased after SATB1 upregulation. SATB1 expression was demonstrated to be positively correlated with liver cancer metastasis. These results indicate that liver cancer metastasis is regulated by SATB1 expression. Thus, immunohistochemical SATB1 expression may present an independent risk factor for the metastasis of liver cancer.

Uterine cervical carcinoma (UCC) is one of the most common malignant tumors in females, and UCC has a close relationship with chronic cervicitis. As the endogenous "braking signal," lipoxins can regulate anti-inflammation and the resolution of inflammation. We investigated the effect of lipoxin A4 (LXA4) on the proliferation, apoptosis, and migration in lipopolysaccharide (LPS)-stimulated Hela cells. We demonstrated that LXA4 could significantly suppress p53, cyclin D1 expression, and migration of LPS-stimulated Hela cells via nuclear factor-κB (NF-κB) pathway, and these effects could be blocked by Boc-2, the specific inhibitor of FPR2/ALX (the receptor of LXA4). We presented evidence for a novel role of LXA4 on the proliferation and migration in LPS-stimulated Hela cells, and FPR2/ALX was involved in the procedures. These results showed that LXA4 could be a possible candidate for UCC therapy, and blocking the activation of NF-κB would be an effective drug target.

There is much evidence suggesting that CCL5 is one of the chemoattractant cytokines involved in diabetes mellitus (DM) with diffuse large B‑cell lymphoma (DLBCL). However, the pathological impact is unclear. In the current study, in order to improve understanding regarding the role of CCL5 in DM with DLBCL, the expression levels of CCL5 mRNA were examined in normal B cells, human DLBCL cell lines (Ly1, Ly8 and Ly10) and a mouse DLBCL cell line (A20), as well as those in cells cultured with either 5 or 30 mmol/l glucose. A20‑CCL5+ (CCL5 overexpression) and A20‑CCL5‑ (CCL5 knockdown) subclones were obtained through cell transduction with a lentiviral vector, and were subcutaneously injected into BALB/c DM mice and normal mice. Tumor growth was observed by calculating the tumor volume. The results demonstrated that CCL5 mRNA levels in DLBCL cells were significantly higher than those in the normal cells (P

Mouse CD99 antigen-like 2 (mCD99L2) has previously been confirmed to be expressed in murine B lymphoma (A20) cells by our group. The present study aimed to establish a mCD99L2‑downregulated A20 cell line and to investigate the effect of shRNA targeting mCD99L2 in A20 cells in vitro and in vivo. Four pLenti6/mCD99L2 expression vectors containing the mCD99L2 shRNA-expressing cassette were constructed, transfected into A20 cells and stable mCD99L2-downregulated A20 subclones, termed A20-mCD99L2- cells, were established and identified by quantitative PCR and western blot analysis. Light and transmission electron microscopy, MTT assay, flow cytometry and immunofluorenscence labeling were used to observe the morphological, biological and phenotypic characteristics in vitro. Some of the A20-mCD99L2- cells exhibited H/RS‑cell like morphology, a decreased proliferative ability, a prolonged G2 phase and increased CD30 and CD15 expression. Upon injecting cells into nude or immunocompetent BALB/c mice, tumorigenesis, tumor growth, morphology and phenotypes in vivo were observed. A20-mCD99L2- cells induced tumors in nude and BALB/c mice, but with less potency in the latter compared with the controls. Similar morphological, biological and phenotypic characteristics were observed in the A20-mCD99L2- cell-induced tumors as those in vitro. Several cytokines including CD30T, IL-12p40/p70, IL-3, IFN-γ, CXCL16, MIP-1α and CD40 were upregulated following mCD99L2 downregulation when detected using antibody arrays. The results from western blot analysis indicated that the regulation of mCD99L2 expression may involve the activated nuclear factor-κB pathway in the murine B lymphoma cells. The present study provides data for further investigation into the mCD99L2 gene in tumor cells.

CCL5 is one of the chemoattractant cytokines involved in inflammatory observed in both diffuse large B-cell lymphoma (DLBCL) and classical Hodgkin's lymphoma (CHL). However, the pathological effects of CCL5 remain unclear. To gain a better understanding of the role of CCL5 in CHL and DLBCL, we examined the expression of CCL5 in the CHL cell line L428 and the DLBCL cell lines Ly1 and Ly8, as well as its chemotactic effect on CD4+ T cells. CCL5 mRNA expression was detected by real-time quantitative RT-PCR. Intracellular CCL5 protein expression was analyzed using confocal microscopy, and CCL5 protein secretion was detected by ELISA. The chemotactic function of CCL5 was assessed using a Transwell coculture system, and the number of migrated CD4+ T cells was counted. Moreover, the p-iкBα and p65 levels of NF-кB signaling molecules in these lymphoma cell lines were detected by Western blotting. The results showed that CCL5 mRNA and protein expression in the L428 cells was significantly higher than in Ly1 and Ly8 cells (p

The healing of diabetic wounds represents a formidable clinical challenge, and the molecular mechanisms involved in diabetic wound healing are far from clear. In this study, we investigated the expression of β-catenin and cyclin D1 in the epidermal stem cells (ESCs) of diabetic rats, and explored whether the reduction of β-catenin and its downstream target in ESCs, cyclin D1, lead to poor wound healing in diabetes mellitus (DM). We found that, compared to the controls, the ESCs of diabetic rats were markedly reduced, the clone formation efficiency of the ESCs was markedly lower, and the mRNA and protein expression of β-catenin and cyclin D1 was significantly decreased. These findings suggest that the low expression of β-catenin and cyclin D1 may reduce the activity of ESCs from diabetic rats, which might be one of the important mechanisms of delayed wound healing in DM.

CD99 is a 32-kDa transmembrane glycoprotein that is encoded by the MIC2 gene. Our study was carried out to examine the role of CD99 in tumor progression of classical Hodgkin lymphoma (cHL). Here, we showed that lowly expressed CD99 protein in cHL cell lines and primary cHL cases correlates with the deficient expression of the positive regulatory domain 1 (PRDM1/BLIMP1). In addition, cHL cell lines showed high levels of miR-9 expression. We determined that the upregulation of CD99 induced expression of transcription factor PRDM1, a master regulator of plasma-cell differentiation, which is also a target for miR-9-mediated downregulation. Indeed, inhibition of miR-9 also triggered upregulation of PRDM1 expression. Furthermore, overexpression of CD99 resulted in changed growth features and reorganization of actin cytoskeleton. As upregulation of CD99 led to a decrease in cHL diagnosis marker CD30 and CD15 and an increase in plasma-cell differentiation marker CD38 and the restoration of B-cell makers PAX5, CD79α and CD19, we suggest that downregulated CD99 leads to the prevention of plasma-cell differentiation in Hodgkin/Reed-Sternberg (H/RS) cells. Furthermore, these data indicate that CD99 may control miR-9 expression, which directly targets PRDM1. Altogether, these results reveal a CD99-miR-9-PRDM1 molecule axis in lymphomagenesis of cHL and suggest that upregulation of CD99 in H/RS cells induces terminal B-cell differentiation, which may provide a novel therapeutic strategies for cHL.

Epidermal stem cells (ESCs) can actively participate in wound healing and enhance reepithelialization. To establish ideal diabetes mellitus (DM) rat models and to investigate the expression of keratin 19 (K19), beta1-integrin, beta-catenin, and proliferating cell nuclear antigen (PCNA) in ESCs of DM rat model, then to study the potential mechanism of difficult recovering wounds of diabetic skin.Twenty male SD rats (weighing 250-300 g) were divided into DM group and normal control group randomly (n=10). The DM rat model was made by intraperitoneal injected 65 mg/kg streptozocin (STZ), the normal control group was not treated. At 4 weeks after injection, pancreatic tissue was harvested for HE staining in two groups. The ESCs isolated from full-thickness skins of the back of two group rats were cultured and identified. The 2nd passage of ESCs were obtained for immunocytochemical staining of K 19, beta1-integrin, beta-catenin, and PCNA. Meanwhile, the cell cycle were measured by flow cytometry. The cell colony formation rates were detected after 1 week.The achievement ratio of DM rat model was 90% with good stability. HE staining showed that the number of islet cells significantly decreased with degeneration and necrosis in DM group; the structure of islet cell was clear without degeneration and necrosis in normal control group. The integral absorbance values of positive expression for K19, beta1-integrin, beta-catenin, and PCNA in ESCs of DM group (82.63 +/- 14.77, 21.59 +/- 4.71, 6.49 +/- 6.58, and 90.77 +/- 12.44, respectively) were significantly lower than those in the normal control group (151.24 +/- 42.83, 54.48 +/- 17.43, 116.39 +/- 9.26, and 110.62 +/- 20.67, respectively) (P0.01). The clone forming efficiency of ESCs in DM group (6.43% +/- 1.01%) was significantly lower than that in the normal control group (11.37% +/- 1.62%) (P0.01). Flow cytometry indicated that 88.89% of cultured ESCs in the DM group were in resting state/pre-DNA-synthetic gap (G0/G1), and the apoptosis rate was 3.98%; 91.50% in the normal control group and the apoptosis rate was 0.The DM rat model can be effectively induced by intraperitoneal injected 65 mg/kg STZ. The decreased amount and the low proliferation and differentiation capacity of ESCs may be one of the important mechanisms of difficult recovering wounds of DM rats.

β-catenin plays an important role in the tissue repair. But its expression and meanings in the diabetic cutaneous wound remains to be determined. In this study, we investigated the expression of β-catenin and PCNA in epidermal stem cells(ESCs) of diabetic rat skin. The diabetes mellitus (DM) rats were induced by a single i.p. injection of streptozotocin. ESCs were extracted from the dorsal skin samples of rats by trypsin digesting method and further purified by collagen adhering methods. Expression of ss1-integrin and keratin 19 were identified as ESCs by immunocytochemical staining . The results showed the amount of β-catenin and PCNA were decreased in ESCs of DM rat skin, and the clone forming efficiency of ESCs in DM rat skin was significantly lower than that in normal skin. It reveals impaired wounds repair in DM is characterized by the protracted epithelialization which is due to a decreased proliferative capacity of epidermal stem cells.