Electroencephalography Microstate Class D is a Brain Marker of Subjective Sleep Quality for College Students with High Habitual Sleep Efficiency.

Subjective sleep quality is an individual's subjective sleep feeling, and its effective evaluation is the premise of improving sleep quality. However, people with autism or mental disorders often experience difficulties in verbally expressing their subjective sleep quality. To solve the above problem, this study provides a non-verbal and convenient brain feature to assess subjective sleep quality. Reportedly, microstates are often used to characterize the patterns of functional brain activity in humans. The occurrence frequency of microstate class D is an important feature in the insomnia population. We therefore hypothesize that the occurrence frequency of microstate class D is a physiological indicator of subjective sleep quality. To test this hypothesis, we recruited college students from China as participants [N = 61, mean age = 20.84 years]. The Chinese version of the Pittsburgh Sleep Quality Index scale was used to measure subjective sleep quality and habitual sleep efficiency, and the state characteristics of the brain at this time were assessed using closed eyes resting-state brain microstate class D. The occurrence frequency of EEG microstate class D was positively associated with subjective sleep quality (r = 0.32, p < 0.05). Further analysis of the moderating effect showed that the occurrence frequency of microstate class D was significantly and positively correlated with subjective sleep quality in the high habitual sleep efficiency group. However, the relationship was not significant in the low sleep efficiency group (ßsimple = 0.63, p < 0.001). This study shows that the occurrence frequency of microstate class D is a physiological indicator of assessing subjective sleep quality levels in the high sleep efficiency group. This study provides brain features for assessing subjective sleep quality of people with autism and mental disorders who cannot effectively describe their subjective feelings.

[Identification and preparation of a glycol-protein fraction AN from tea extracts and its in vivo and in vitro anti-hyperglycosemia activity].

The present study compared active ingredients of tea from different sources to select tea type and the fraction of tea extracts for the highest anti-hyperglycemic activity, and to verify anti-hyperglycemic activity of the selected tea extract. Tea extracts were separated and enriched by molecular weight using ultra-filtration technology. The extracts were first screened by α-glucosidase inhibition assay, followed by using a rat inverted intestine sac system to measure the effect on glucose transport. Both alloxan-induced diabetic rat model and high-fat diet combined with streptozotocin-induced rat diabetes mellitus model were used to study the effects of active components on blood glucose, body weight, insulin resistance. The experimental results showed that the different kinds of tea extracts had different inhibitory effects on α-glucosidase, and the inhibitory effect of tea extract E on α-glucosidase was stronger. The effects of different components of tea extract E also varied greatly, of which Fraction AN protein had stronger inhibitory effect on α-glucosidase than other fragments, and Fraction AN protein had a strong inhibitory effect on glucose transport, reduced blood sugar and normalized insulin secretion in diabetic rats. The results suggest that a glycol-protein fraction(AN) from the extracts might be responsible for the anti-hyperglycemic activity of tea polysaccharides. The AN glycol-protein fraction has strong inhibitory effects on both α-glucosidase activity and glucose transport by the small intestine. It also reduced blood glucose level and normalized insulin secretion in diabetic rats, and has a protective effect on diabetic rats.

[Clinical study of double plate system in the treatment of complex proximal humeral fractures in the elderly].

OBJECTIVE: To explore the clinical outcomes of anteromedial combined with lateral locking plate for complex proximal humeral fractures in the eldery. METHODS: From June 2018 to October 2020, 30 patients who underwent surgical treatment for Neer grade 3 to 4 proximal humeral fractures, including 8 males and 22 females, aged from 51 to 78 years old with an average of (61.5±7.5) years old. Of them, 15 patients had fractures fixed with anteromedial combined with lateral locking plate(ALLP group), whereas 15 received internal fixation with proximal humerus locking plate only(PHLP group). The clinical data, simple shoulder test (SST), humeral head height loss, varus angle and shoulder range of motion were compared between the two groups. RESULTS: All fractures were healed. The follow-up time ranged from 12 to 24 months, with an average of(14.3±2.9) months. The operation time of ALLP group was longer than that of PHLP group (P<0.05). There was no significant difference in intraoperative blood loss between the two groups (P>0.05). There was no significant difference in SST score between the two groups at 1, 3 and 12 months after operation (P>0.05). In terms of radiographic measurement, there was no significant difference in humeral head height loss and varus angle between the two groups at 1 and 3 months after operation (P>0.05). At 12 months after operation, the height loss and varus angle of humeral head in ALLP group were lower than those in PHLP group (P<0.05). In shoulder range of motion, the range of forward elevation in ALLP group was larger than that in PHLP group 1 year after operation(P<0.05). There was no significant difference in external rotation between the two groups. CONCLUSION: Anteromedial combined with lateral locking plate in the treatment of complex proximal humeral fractures in the elderly can increase the stability of the medial column and obtain a good fracture prognosis. But there are also disadvantages such as longer operation time, so it should be individualized according to the fracture type of the patient.

[Retracted] Inhibition of δ­opioid receptors induces brain glioma cell apoptosis through the mitochondrial and protein kinase C pathways.

[This retracts the article DOI: 10.3892/ol.2013.1546.].

Atp8a1 deletion increases the proliferative activity of hematopoietic stem cells by impairing PTEN function.

PURPOSE: The eukaryotic cell plasma membrane contains several asymmetrically distributed phospholipids, which is maintained by the P4-ATPase flippase complex. Herein, we demonstrated the biological effects and mechanisms of asymmetrical loss in hematopoietic stem cells (HSCs). METHODS: An Atp8a1 knockout mouse model was employed, from which the HSC (long-term HSCs and short-term HSCs) population was analyzed to assess their abundance and function. Additionally, competitive bone marrow transplantation and 5-FU stress assays were performed. RNA sequencing was performed on Hematopoietic Stem and Progenitor Cells, and DNA damage was assayed using immunofluorescence staining and comet electrophoresis. The protein abundance for members of key signaling pathways was confirmed using western blotting. RESULTS: Atp8a1 deletion resulted in slight hyperleukocytosis, associated with the high proliferation of HSCs and BCR/ABL1 transformed leukemia stem cells (LSCs). Atp8a1 deletion increased the repopulation capability of HSCs with a competitive advantage in reconstitution assay. HSCs without Atp8a1 were more sensitive to 5-FU-induced apoptosis. Moreover, Atp8a1 deletion prevented HSC DNA damage and facilitated DNA repair processes. Genes involved in PI3K-AKT-mTORC1, DNA repair, and AP-1 complex signaling were enriched and elevated in HSCs with Atp8a1 deletion. Furthermore, Atp8a1 deletion caused decreased PTEN protein levels, resulting in the activation of PI3K-AKT-mTORC1 signaling, further increasing the activity of JNK/AP-1 signaling and YAP1 phosphorylation. CONCLUSION: We identified the role of Atp8a1 on hematopoiesis and HSCs. Atp8a1 deletion resulted in the loss of phosphatidylserine asymmetry and intracellular signal transduction chaos.

Thymoquinone inhibits growth and augments 5-fluorouracil-induced apoptosis in gastric cancer cells both in vitro and in vivo.

Thymoquinone (TQ), a component derived from the bioactive constituent of black seed (Nigella sativa), has been shown to exert biological activity on various types of human cancers. However, there are few studies addressing its effects on gastric cancer. Here, we present the first report describing the chemosensitizing effect of thymoquinone and 5-fluorouracil (5-FU) on gastric cancer cells both in vitro and in vivo. Studies have shown that pretreatment with TQ significantly increased the apoptotic effects induced by 5-FU in gastric cancer cell lines in vitro. Moreover, we found that TQ enhanced the 5-FU-induced killing of gastric cancer cells by mediating the downregulation of the anti-apoptotic protein bcl-2, the upregulation of the pro-apoptotic protein bax, and the activation of both caspase-3 and caspase-9. In addition to the in vitro results, it has been shown that the combined treatment of TQ with 5-FU represents a significantly more effective antitumor agent than either agent alone in a xenograft tumor mouse model. These data suggest that the TQ/5-FU combined treatment induces apoptosis by enhancing the activation of both caspase-3 and caspase-9 in gastric cancer cells. These results, which provide molecular evidence both in vitro and in vivo, support our conclusion that thymoquinone can activate caspase-3 and caspase-9 and thus result in the chemosensitisation of gastric cancer cells to 5-FU-induced cell death.

Noscapine induces mitochondria-mediated apoptosis in human colon cancer cells in vivo and in vitro.

Noscapine, a phthalide isoquinoline alkaloid derived from opium, has been widely used as a cough suppressant for decades. Noscapine has recently been shown to potentiate the anti-cancer effects of several therapies by inducing apoptosis in various malignant cells without any detectable toxicity in cells or tissues. However, the mechanism by which noscapine induces apoptosis in colon cancer cells remains unclear. The signaling pathways by which noscapine induces apoptosis were investigated in colon cancer cell lines treated with various noscapine concentrations for 72 h, and a dose-dependent inhibition of cell viability was observed. Noscapine effectively inhibited the proliferation of LoVo cells in vitro (IC(50)=75 µM). This cytotoxicity was reflected by cell cycle arrest at G(2)/M and subsequent apoptosis, as indicated by increased chromatin condensation and fragmentation, the upregulation of Bax and cytochrome c (Cyt-c), the downregulation of survivin and Bcl-2, and the activation of caspase-3 and caspase-9. Moreover, in a xenograft tumor model in mice, noscapine injection clearly inhibited tumor growth via the induction of apoptosis, which was demonstrated using a TUNEL assay. These results suggest that noscapine induces apoptosis in colon cancer cells via mitochondrial pathways. Noscapine may be a safe and effective chemotherapeutic agent for the treatment of human colon cancer.

Thymoquinone prevents and ameliorates dextran sulfate sodium-induced colitis in mice.

BACKGROUND: Thymoquinone (TQ), an active ingredient of the seed oil extract of Nigella sativa Linn, has previously been shown to possess antitumor, antioxidant, and anti-inflammatory bioactivity. Whether TQ has any effect on colitis remains controversial. AIM: The aim of this study was to determine whether treatment with TQ prevents and ameliorates colonic inflammation in a mouse model of inflammatory bowel disease. METHODS: C57BL/6 murine colitis was induced by the administration of dextran sodium sulfate (DSS) (3 % W/V) in the drinking water supplied to the mice for 7 consecutive days. The mice with colitis were treated with 5, 10, or 25 mg/kg TQ orally, and changes in body weight and macroscopic and microscopic colitis scores were examined. In addition, biochemical analyses were conducted. RESULTS: The treatment of mice with TQ prevented and significantly reduced the appearance of diarrhea and body weight loss. These results were associated with amelioration of colitis-related damage, as measured by macroscopic and microscopic colitis scores. In addition, there was a significant reduction in colonic myeloperoxidase activity and malondialdehyde levels and an increase in glutathione levels. CONCLUSIONS: These results indicate that TQ administration can prevent and improve murine DSS-induced colitis. These findings suggest that TQ could serve as a potential therapeutic agent for the treatment of patients with inflammatory bowel disease.

Low-dose cyclophosphamide combined with IL-2 inhibits tumor growth by decreasing regulatory T cells and increasing CD8+ T cells and natural killer cells in mice.

Interleukin-2 (IL-2) benefits some cancer patients by promoting the proliferation of cytotoxic effector T cells, but this process is limited by the expansion of regulatory T cells (Tregs). Low-dose cyclophosphamide (CTX) can inhibit the number and function of Tregs. We treated carcinoma-bearing mice with Vehicle, CTX, IL-2 and CTX + IL-2 to investigate the effects of low-dose CTX combined with IL-2 in antitumor treatment. In comparison to monotherapy, CTX + IL-2 significantly limited tumor growth, via tumor cell proliferation inhibition and increased apoptosis. The infiltration of CD8+ T cells in tumor tissues was significantly increased in the CTX + IL-2 group. CTX + IL-2 safely increased CD8+ T and natural killer cells in the spleen, lymph nodes and peripheral blood, and CTX attenuated the increase in Tregs induced by IL-2 in the spleen.

Exploring the Relationship Between Trait Mindfulness and Interpersonal Sensitivity for Chinese College Students: The Mediating Role of Negative Emotions and Moderating Role of Effectiveness/Authenticity.

Background: Interpersonal sensitivity is a prominent mental health problem facing college students today. Trait mindfulness is a potential positive factor that may influence interpersonal relationships. However, the precise relationship between trait mindfulness and interpersonal sensitivity remains elusive, which limits the optimization and further application of mindfulness-based intervention schemes targeting interpersonal sensitivity. This study aimed to explore (a) whether negative emotions mediate the relationship between trait mindfulness and interpersonal sensitivity and (b) whether the relationship among trait mindfulness, negative emotions, and interpersonal sensitivity is moderated by effectiveness/authenticity. We hypothesize that (a) negative emotions mediate the relationship between trait mindfulness and interpersonal sensitivity, and (b) effectiveness/authenticity moderates the indirect association between trait mindfulness and interpersonal sensitivity through negative emotions. Methods: One thousand four hundred nineteen Chinese college students (1,023 females, 396 males), aged from 17 to 23 (SD = 0.86, mean = 18.38), participated in this study. Their trait mindfulness, negative emotions, the effectiveness/authenticity, and interpersonal sensitivity were measured using well-validated self-report questionnaires. Results: Correlational analyses indicated that both trait mindfulness and effectiveness/authenticity were significantly and negatively associated with interpersonal sensitivity. Mediation analyses uncovered a partial mediating role of negative emotions in the relationship between trait mindfulness and interpersonal sensitivity. Moderated mediation analyses showed that in college students with high effectiveness/authenticity, the relationship between trait mindfulness and negative emotions was stronger, whereas the relationship between negative emotions and interpersonal sensitivity was weaker. Conclusion: Negative emotion is a mediator of the relationship between trait mindfulness and interpersonal sensitivity, which in turn is moderated by effectiveness/authenticity. These findings suggest a potential mechanism through which trait mindfulness influences interpersonal sensitivity. Mindfulness-based interventions have the potential to decrease interpersonal sensitivity and offer a basis for predicting individual differences in response to mindfulness-based interventions among individuals.

[Expression of Dickkopf-3 in esophageal squamous cell carcinoma].

OBJECTIVE: To investigate the expression of Dickkopf-3 (Dkk-3) in esophageal cancer and normal esophageal tissue and the relationship between Dkk-3 expression and the biological behavior of esophageal cancer. METHODS: Immunohistochemical method of S-P was used to examine Dkk-3 expression in 69 cases of esophageal squamous cell carcinoma and 5 cases of normal esophageal tissue with non-tumor tissue microarray and the results were analyzed and correlated with their clinical and pathological features. RESULTS: Positive Dkk-3 expression was observed in 65.7% (44/67) of the esophageal squamous cell carcinoma cases, but only one of the five cases with normal esophageal tissue showed positive microvascular expression of Dkk-3. In cases with positive expression of Dkk-3 significant differences were found in fiber membrane infiltration, depth of invasion, lymph node metastasis and TNM staging (P < 0.05), while no significant differences were found in the age, gender and pathological grading (P > 0.05). CONCLUSIONS: The upregulation of Dkk-3 expression in esophageal squamous cell carcinoma may contribute to tumor invasion and metastasis.

Relationship Between Trait Mindfulness and Sleep Quality in College Students: A Conditional Process Model.

Sleep quality can affect the physical and mental health, as well as the personal development of college students. Mindfulness practices are known to ameliorate sleep disorder and improve sleep quality. Trait mindfulness, an innate capacity often enhanced by mindfulness training, has been shown to relate to better sleep quality and different aspects of psychological well-being. However, how individual difference factors such as trait mindfulness relate to sleep quality remains largely unclear, which limits the optimization and further application of mindfulness-based intervention schemes targeting the improvement of sleep quality. In this study, we aimed to investigate how negative emotions and neuroticism may influence the relationship between trait mindfulness and sleep quality. A conditional process model was built to examine these relationships in 1,423 Chinese young adults. Specifically, the conditional process model was constructed with trait mindfulness as the independent variable, sleep quality as the dependent variable, negative emotions as the mediating variable, and neuroticism as the moderating variable. Our results showed that negative emotions mediated the link between mindfulness and sleep quality and that neuroticism had a moderating effect on the relationship between mindfulness and sleep quality. Together, these findings suggested a potential mechanism of how trait mindfulness influences sleep quality, provided a therapeutic target for which mindfulness-based interventions may act upon to improve sleep quality, and offered a basis for prediction of different intervention effects among individuals.

miR-424-5p Regulates Hepatoma Cell Proliferation and Apoptosis.

OBJECTIVE: Yes-associated protein (Yes-associated protein 1 [YAP1]) is an important oncogene that is related to the pathogenesis and progression of liver cancer. It was found that miR-424-5p expression was significantly decreased in liver cancer tissues, revealing its anticancer effect. Bioinformatic analysis demonstrated the targeted relationship between miR-424-5p and the 3' untranslated region of YAP1. This study investigated the role of miR-424-5p in regulating YAP1 expression and affecting hepatoma cell proliferation and apoptosis. MATERIALS AND METHODS: Tumors and normal liver tissues adjacent to tumors were collected from patients to detect the expression of miR-424-5p and YAP1. A dual-luciferase reporter gene assay was adopted to explore the targeted regulation between miR-424-5p and YAP1. Liver cancer HCCLM3 and MHCC97-L cells and normal liver HL-7702 cells were cultured in vitro to compare expression levels of miR-424-5p and YAP1. HCCLM3 and MHCC97-L cells were divided into the miR-NC group and miR-424-5p mimic group. Cell apoptosis was detected by flow cytometry. Cell proliferation was determined by EdU staining. RESULTS: Compared with normal liver tissue, miR-424-5p expression was significantly decreased, while YAP1 mRNA and protein levels were obviously upregulated in liver cancer tissues, which were related to the clinical stage. A negative correlation was found between miR-424-5p and YAP1 mRNA levels in liver cancer tissues. Dual-luciferase reporter gene assay confirmed the targeted relationship between miR-424-5p and YAP1. miR-424-5p expression in HCCLM3 and MHCC97-L cells decreased compared with L20 cells, which correlated with malignancy. YAP1 level in HCCLM3 and MHCC97-L cells was significantly enhanced, which correlated with malignancy. miR-424-5p mimic transfection significantly downregulated YAP1 expression in HCCLM3 and MHCC97-L cells, resulting in enhanced apoptosis and attenuated cell proliferation. CONCLUSIONS: Decreased miR-424-5p expression and increased YAP1 expression are found in patients with liver cancer. Increased miR-424-5p can inhibit YAP1 expression, attenuate hepatoma cell proliferation, and induce cell apoptosis.

Silencing of FRAT1 by siRNA inhibits the proliferation of SGC7901 human gastric adenocarcinoma cells.

Frequently rearranged in advanced T cell lymphomas-1 (FRAT1) positively regulates the Wnt/ß-catenin signaling pathway by inhibiting glycogen synthase kinase-3 mediated phosphorylation of ß-catenin. FRAT1 is a proto-oncogene, implicated in tumorigenesis. The present study aimed to investigate the effects of FRAT1 silencing on the proliferation and apoptosis of SGC7901 cells. FRAT1 in SGC7901 cells was silenced by RNA interference. Reverse transcription-quantitative polymerase chain reaction was used for the analysis of FRAT1 mRNA and western blotting was used to evaluate FRAT1 and ß-catenin protein levels. Cell proliferation was analyzed by the MTT assay. Cell cycle distribution and apoptosis were analyzed by flow cytometry. The expression of FRAT1 mRNA, FRAT1 and ß-catenin protein in FRAT1-silenced SGC7901 cells were reduced significantly compared to untreated cells. The proliferation of FRAT1 silenced SGC7901 cells decreased significantly The FRAT1 silenced SGC7901 cells were arrested at G0/G1 stage to a greater degree, and apoptosis was increased. In summary, silencing of FRAT1 inhibits SGC7901 cell proliferation and induces apoptosis, possible through a reduction in ß-catenin expression. FRAT1 may serve as a prognostic biomarker and therapeutic target for gastric cancer.

Synergistic antitumor effect of puerarin combined with 5-fluorouracil on gastric carcinoma.

Combination chemotherapy is a crucial method in the treatment of gastric cancer. The aim of the present study was to investigate the inhibitory effects of puerarin and 5­fluorouracil (5­FU) on BGC­823 gastric cancer cells in vitro and in vivo. The in vitro growth inhibition of puerarin or 5­FU alone or combined on BGC­823 cells was determined using a cell counting kit 8 (CCK­8) on living cells. Apoptotic morphological features and proteins expression levels were detected by Hoechst 33258 staining, an Annexin V/propidium iodide apoptosis kit and western blot analysis, respectively. Tumor xenografts were established in nude mice and the inhibitory effects and side effects were detected. Results of the CCK­8, Hoechst 33258 staining and flow cytometry revealed that the combined treatment was more effective than the separate treatments. The tumor volume was 90.65% of that of the controls and the mean tumor weight was only 0.125 g at the end of the experiment in the combination group compared with the control group (0.822 g). In addition, it was determined that liver and renal toxicity did not increase in combined treatment. These findings showed that puerarin and 5­FU produced a significant synergic effect on gastric cancer cells, while there was no increase in side effects.

Synergistic effect of puerarin and 5-fluorouracil on hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common types of human malignancy worldwide, which is becoming increasingly resistant to traditional drug treatments. Puerarin combined with 5-fluorouracil (5-FU) may be a useful treatment for liver cancer. The primary aim of the present study was to determine whether combined treatment with 5-FU and puerarin is more effective against the hepatocellular carcinoma (HCC) cell line, SMMC7721, than treatment with 5-FU or puerarin alone. The growth inhibition of SMMC7721 cells by puerarin or 5-FU alone or in combination was determined by the Cell Counting Kit-8 assay, in vitro. Apoptotic morphological features and the percentage of apoptotic cells were detected using Hoechst 33258 staining and an Annexin V/PI apoptosis kit, respectively. In addition, a tumor xenograft model was established in nude mice using SMMC7721 cells. Puerarin and 5-FU alone or in combination were injected into the mice, and the inhibition of tumor growth was evaluated by monitoring tumor volume and weight. Treatment with 6,400 or 640 µM 5-FU resulted in growth inhibition of 95.56±0.81 and 75.91±3.54%, respectively. The combination index values were <1 when the fraction of affected cells was between 0.2555 and 0.7420. Furthermore, the percentage of apoptotic cells was markedly increased in the combined treatment group when compared with that of the individual treatment groups, in vitro and in vivo. Individual treatment with puerarin resulted in a tumor volume inhibition rate (IR) of 70.58% and a tumor weight IR of 46.20%. Treatment with 5-FU was found to decrease the tumor volume by 76.26% and tumor weight by 49.86%. In the combined treatment group, the tumor volume and weight IRs were 93.11 and 75.21%, respectively. A marked increase in the inhibition of tumor growth and the number of apoptotic cells in response to combined treatment with puerarin and 5-FU was identified with no observed liver or renal toxicity. These results suggest that puerarin and 5-FU exhibit a synergistic treatment effect on the HCC SMMC7721 cell line.

Synergistic effects of puerarin combined with 5-fluorouracil on esophageal cancer.

Puerarin is an isoflavone derived from kudzu roots with a wide range of biological and medicinal properties. The aim of the present study was to investigate the inhibitive effects of puerarin combined with 5­fluorouracil (5­FU) on Eca­109 esophageal cancer cells in vitro and in vivo. Inhibitive effects of the treatments on Eca­109 cells were detected by cell counting kit­8, Hoechst 33258 staining and flow cytometry. A tumor xenograft model was established in nude mice. Puerarin and 5­FU, administered either in combination or individually, were injected into mice and the inhibitive effects along with any side effects were observed. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Puerarin and 5­FU, administered as combined treatment or individual drugs, significantly inhibited proliferation and induced marked apoptosis. The mean growth inhibition rate (± standard deviation) reached 87.27±5.37% and the apoptotic rate at 48 h reached 36.18±1.24% in the combined treatment group. The percentages of apoptotic cells induced by puerarin and 5­FU (combined or alone) were significantly higher than those of the control group (P<0.05). Puerarin or 5­FU alone significantly inhibited the growth of xenograft tumors in comparison to the control group (P<0.05), with inhibition rates of 76.93 and 72.21%, respectively. The drugs combined exhibited a significantly greater effect than either drug alone (P<0.05), with the tumor inhibition rate reaching 89.06%. During the course of chemotherapy, no evident side effects were observed. The results suggested that the combined inhibitive effects of puerarin and 5­FU were greater than the effects of the agents used individually. In addition, puerarin combined with 5­FU exhibited synergistic effects at lower concentrations and promoted apoptosis, but did not increase the side effects of chemotherapy, which indicated that puerarin may be a safe and effective chemosensitive agent in the treatment of human esophageal cancer.

Potential effects of Mina53 on tumor growth in human pancreatic cancer.

Myc-induced nuclear antigen (Mina53) is a protein with a molecular weight of 53 kDa expression of which is induced by c-Myc. Increased expression of Mina53 is documented in some human carcinomas. In this study, we found markedly increased Mina53 expression in pancreatic cancer tissue specimens. This expression did not correlate with clinicopathological characteristics, such as sex, age, and presence of distant metastasis. However, there was a statistically significant association with histological differentiation, TNM stage, and lymph node metastases. To study functional role of Mina53, we silenced its expression by siRNA in PANC-1 cells. These cells were arrested in the G2/M phase, and apoptosis rates were increased. In conclusion, increased expression of Mina53 may play an important role in the development of human pancreatic cancer. Mina53 can be used as a marker for pancreatic cancer and may potentially be exploited as a target for treatment of pancreatic cancer.

Suppressive effect of sinomenine combined with 5-fluorouracil on colon carcinoma cell growth.

It is reported that sinomenine (SIN) and 5-fluorouracil (5-FU) both are effective for colon cancer, but their cooperative suppressive effects and toxicity remain to be clarified in detail. This study aimed to determine suppressive effects and toxicity of sinomenine (SIN) plus 5-fluorouracil (5-FU) on LoVo colon carcinoma cells in vitro and in vivo. CCK-8, Hoechst 33258 staining and an annexin V-FITC/PI apoptosis kit were used to detect suppressive effects. Western blotting was applied to investigate the essential mechanism underlying SIN and 5-FU-induced apoptosis. SIN or 5-FU or both were injected into nude mice, and then suppressive effects and side effects were observed. SIN plus 5-FU apparently inhibited the proliferation of LoVo cells and induced apoptosis. Moreover the united effects were stronger than individually (p<0.05). The results of annexin V-FITC /PI staining and Hoechst 33258 staining showed that the percentage of apoptotic cells induced by SIN and 5-FU combined or alone was significantly higher than the control group (p<0.05). Expression of Bax and Bcl-2 was up-regulated and down-regulated respectively. SIN or 5-FU significantly inhibited effects on the volume of tumour xenografts and their combined suppressive effects were stronger (p<0.05). No obvious side effects were observed. It was apparent that the united effects of SIN and 5-FU on the growth of colorectal carcinoma LoVo cells in vitro and in vivo were superior to those using them individually, and it did not markedly increase the side effects of chemotherapy.