Correction for ‘Simultaneous and combined detection of multiple tumor markers for cancer screening in human serum by an upgraded photonic crystal-encoded suspension array’ by Shiya Zheng et al., RSC Adv., 2016, 6, 92267–92275.
To investigate the relationship of the expression of vasodilator-stimulated phosphoprotein (VASP) with the metastasis and prognosis of prostate cancer.Prostate cancer PC3 cells were infected with VASP shRNA and control shRNA lentiviruses, respectively. The invasive ability of the PC3 cells was determined by transwell migration assay, the expression of VASP in the prostate cancer tissue from 56 patients was detected by immunohistochemistry, and the survival rate of the patients was analyzed according to the VASP expression levels and follow-up data after radical prostatectomy.VASP shRNA lentivirus significantly inhibited the expression of VASP and decreased the invasive ability of the PC3 cells as compared with the results obtained in the scramble shRNA and blank control groups (P<0.05). The survival analysis of the 56 prostate cancer patients showed that the time of biochemical recurrence was markedly shorter in the VASP positive and strongly positive groups than in the VASP-negative cases (P<0.05), but with no statistically significant difference between the former two groups (P>0.05).VASP is involved in the regulation of the invasive ability of prostate cancer PC3 cells, and the differences in the VASP expression are related to the prognosis of prostate cancer.目的： 研究血管扩张刺激磷蛋白（VASP）与前列腺癌侵袭转移及预后的关系。 方法： 将VASPshRNA慢病毒和对照shRNA慢病毒分别感染前列腺癌PC3细胞，采用跨膜迁移实验检测PC3细胞的侵袭能力；采用免疫组化法检测56例前列腺癌患者癌组织中VASP的表达，并根据VASP表达差异及患者前列腺癌根治术后随访结果进行生存分析比较。结果： 与shRNA慢病毒对照组及空白对照组相比，VASPshRNA慢病毒可抑制前列腺癌PC3细胞VASP的表达，并且显著降低PC3细胞的侵袭能力（P<0.05）；对56例前列腺癌患者的生存分析表明，与VASP阴性表达组相比，VASP阳性表达组及VASP强阳性表达组患者生化复发时间显著缩短（P<0.05），后两者之间比较差异无统计学意义（P>0.05）。结论： VASP参与调控前列腺癌PC3细胞的侵袭能力；VASP蛋白表达差异与前列腺癌患者的预后相关。.
Erythropoietin‑producing hepatocellular (Eph) receptors and their ligand ephrins serve crucial roles in the interactions among epithelial cells. Eph receptor/ephrin signaling regulates cell functions, including proliferation, differentiation and migration, via these cell‑cell interactions. We reported previously that EPHB2, a member of the Eph receptor family, was highly expressed in chemically induced cutaneous squamous cell carcinoma (cSCC) tissues in mice. Although the higher expression level of EPHB2 has been observed in various human cancers, its roles in the development and progression of cancers are still unclear. In the present study, the functional implications of EPHB2 in the acquisition of malignant phenotypes of cSCC cells was investigated. Silencing of EPHB2 in the human cSCC cell line A431 induced epithelial‑mesenchymal transition (EMT)‑like morphological changes accompanied by a significant upregulation of epithelial‑mesenchymal transition‑associated genes such as zinc finger E‑box binding homeobox 1/2. In addition, silencing of EPHB2 suppressed anchorage‑independent cell growth under 3D culture conditions. Consistent with these observations, EPHB2 exhibited higher levels of expression in tumor spheres formed under 3D culture conditions than in cells cultured in adherent form, and the expression pattern of EMT markers indicated that EMT was suppressed in tumor spheres. The results of the present study indicated that EPHB2 serves a pivotal role in promoting the anchorage‑independent growth of A431 cells through the suppression of EMT.
Although platinum‑based chemotherapy is the first‑line choice for locally advanced or metastatic esophageal squamous cell carcinoma (ESCC) patients, accelerated recurrence and chemoresistance remain inevitable. New evidence suggests that metabolism reprogramming under stress involves independent processes that are executed with a variety of proteins. This study investigated the functions of nutrient stress (NS)‑mediated acetyl‑CoA synthetase short‑chain family member 2 (ACSS2) in cell proliferation and cisplatin‑resistance and examined its combined effects with proliferating cell nuclear antigen (PCNA), a key regulator of DNA replication and repair. Here, it was demonstrated that under NS, when the AMP‑activated protein kinase (AMPK) pathway was activated, ESCC cells maintained proliferation and chemoresistance was distinctly upregulated as determined by CCK‑8 assay. As determined using immunoblotting and RT‑qPCR, compared with normal esophageal epithelial cells (Het‑1A), ESCC cells were less sensitive to NS and showed increased intracellular levels of ACSS2. Moreover, it was shown that ACSS2 inhibition by siRNA not only greatly interfered with proliferation under NS but also participated in DNA repair after cisplatin treatment via PCNA suppression, and the acceleration of cell death was dependent on the activation of the AMPK pathway as revealed by the Annexin V/PI and TUNEL assay results. Our study identified crosstalk between nutrient supply and chemoresistance that could be exploited therapeutically to target AMPK signaling, and the results suggest ACSS2 as a potential biomarker for identifying higher‑risk patients.
In the present paper, the binding reaction between meso-tetra-(4-hydroxyphenyl)-Zn porphyrin (TPP-Zn) and bovine serum albumin (BSA) was studied at different temperatures by fluorescence method. It was shown that meso-tetra-(4-hydroxyphenyl)-Zn porphyrin has a strong ability of quenching the fluorescence of bovine serum albumin. Based on the mechanisms of fluorescence quenching of bovine serum albumin caused by meso-tetra-(4-hydroxyphenyl)-Zn porphyrin, the binding constants between meso-tetra-(4-hydroxyphenyl)-Zn porphyrin and bovine serum albumin were measured under different temperatures. The experiment showed that meso-tetra-(4-hydroxyphenyl)-Zn porphyrin and bovine serum albumin have strong interactions. The binding constants of the reaction at 27 degrees C, 35 degrees C and 42 degrees C were 1.521 x 10(6) L x mol(-1), 7.048 x 10(5) L x mol(-1) and 1.473 x 10(5) L x mol(-1), respectively, and were decreased with increasing the temperature. The constants of maximum diffusion collision quenching rate-K(q) were above 2.0 x 10(10) L x mol(-1) x s(-1). Therefore, the sort of quenching between meso-tetra-(4-hydroxyphenyl)-Zn porphyrin and bovine serum albumin was determined as static quenching. By the theory of Forster of non-radiation energy transfer, the binding distance and the energy transfer efficiency at 27 degrees C between meso-tetra-(4-hydroxyphenyl)-Zn porphyrin (accepter of energy) and bovine serum albumin (donor of energy) were obtained, respectively. The binding distance was 3.72 nm, which is less than 7 nm, therefore, the interaction was similar to the non-radiation energy transfer, and the static quenching was further proved. According to the thermodynamic parameters, the main sorts of binding force between meso-tetra-(4-hydroxyphenyl)-Zn porphyrin and bovine serum albumin could be judged as electrostatic force when deltaG 0.
Objective
To investigate the effect of eicosapentaenoic acid(EPA) on the apoptosis of human colon cancer SW480 cells and the mechanisms.
Methods
Mitochondrial membrane potential was detected, the quantity of cytochrome C was analyzed by Elisa kit, and the expression of cleaved caspase-9 and caspase-3 was detected by Western Blot.
Results
After treatment with EPA(0μg/mL, 42.1μg/mL, 84.2μg/mL, 168.4μg/mL), the mitochondrial membrane potential(Δψm) of SW480 cells were declined(P<0.05), the values were (99.71±0.04)%, (95.04±0.10)%, (88.65±0.41)% and (73.60±1.20)%(t=5.161, 6.302, 4.601, 5.198, all P<0.05). The quantity of cytochrome C in cytosol was increased significantly compared with no treatment group, and the values were (12.8±1.2)ng/mL, (115.5±3.5)ng/mL, (290.5±5.2)ng/mL and (262.0±12.5)ng/mL in different EPA treatment groups(t=6.345, 6.013, 5.846, 4.613, all P<0.01). The expression of cleaved caspase-9 and caspase-3 were significantly increased.
Conclusion
EPA inhibits SW480 cells growth and induces apoptosis in a dose dependent manner.This action may be mediated by mitochondria-mediated intrinsic apoptosis pathway, cytochrome C release, and caspase-9 and caspase-3 activation.
Key words:
Colon tumor; Twenty carbon five acid; SW480 cells; Cell apoptosis
The contribution of individual and combined inflammatory markers for the prognosis of acute ischemic stroke (AIS) remains elusive. This study investigated the effect of systemic inflammatory response index (SIRI), and neutrophil to high-density lipoprotein ratio (NHR), which is mediated by fasting blood glucose (FBG), on 90-day prognosis of patients with AIS.
The relationship between insulin resistance-related indices and the outcomes of acute ischemic stroke (AIS) is still unclear. This study aimed to explore the association between the Apo B/Apo A-1 ratio and the Prognostic Nutritional Index (PNI) with the 90-day outcomes of AIS.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)