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Biomimetic kind of graphdiyne reinforced hemin for enhanced peroxidase-like activity.
Studies have shown that suppression of both the JAK/STAT3 pathway and epithelial‑mesenchymal transition (EMT) may overturn the resistance of non‑small cell lung cancer (NSCLC) cells to gefitinib. Zoledronic acid (ZA) injection is used to treat and prevent multiple forms of osteoporosis, hypercalcemia and bone metastasis‑related complications of malignancy. Clinical research has shown that ZA may exert antitumour effects and delay the progression of NSCLC. In the present study, we investigated whether ZA combined with gefitinib could re‑sensitise NSCLC cells to gefitinib in vitro and in vivo through inhibition of the JAK/STAT3 signalling pathway and EMT reversal. The results revealed that ZA potently increased the sensitivity of gefitinib‑resistant lung cancer cells to gefitinib. ZA decreased activation of JAK/STAT3 signalling and reversed EMT in the H1975 and HCC827GR cell lines. Furthermore, addition of IL‑6 to ZA‑pretreated gefitinib‑resistant cell lines abrogated the effect of ZA and restored the cellular resistance to tyrosine kinase inhibitors. Finally, ZA‑based combinatorial therapy effectively inhibited the growth of xenografts derived from gefitinib‑resistant cancer cells, which was correlated with the inhibition of the JAK/STAT3 signalling pathway and EMT reversal. In conclusion, ZA re‑sensitised gefitinib‑resistant lung cancer cells through inhibition of the JAK/STAT3 signalling pathway and EMT reversal. The combination of ZA and gefitinib may be a promising therapeutic strategy to reverse gefitinib resistance and prolong the survival of patients with NSCLC.Following the publication of the above article, the authors have realized that Fig. 5A was published with certain errors; essentially, the authors needed to perform further experiments to validate certain of their results, and the Blank and si‑NC control data in Fig. 5A were included from an incorrect set of experiments (the intended si‑NUSAP1 experimental data from the flow cytometric analyses, however, were presented correctly in the published Figure). The corrected version of Fig. 5, featuring the panels for the Blank and si‑NC control data in Fig. 5A from the same set of experiments, is shown opposite. The authors have confirmed that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum. Furthermore, they apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Oncology Reports 36 1506-1516, 2016; DOI 10.3892/or.2016.4955].Orf virus (ORFV) is a favorable oncolytic viral carrier in research, and ORFV strain NZ2 has been revealed to have antitumor effects in animal models mediated by immunoregulation profile. However, the antitumor effects triggered by the ORFV in colorectal cancer (CRC) cells is poorly characterized. The in vivo and in vitro roles of ORFV in CRC were determined using western blotting, colony formation, CCK‑8, wound scratch assay, qPCR, and animal models. Furthermore, cytokine antibody chip assay, flow cytometry, western blotting, and immunohistochemical (IHC) assays were conducted to explore the potential mechanism of ORFV. The present data revealed that ORFV strain NA1/11 infected and inhibited the in vitro growth and migration of CRC cells. By establishing a CRC model in Balb/c mice, it was revealed that ORFV strain NA1/11 significantly inhibited the in vivo growth and migration of CRC cells. A cytokine antibody array was utilized to obtain a more comprehensive profile revealing the differentially expressed cytokines in ORFV infection. Cytokines, such as IL‑7, IL‑13, IL‑15, CD27, CD30, pentraxin 3, and B lymphocyte chemoattractant (BLC), were upregulated. Axl, CXCL16, ANG‑3, MMP10, IFN‑γ R1 and VEGF‑B were downregulated. The results indicated that ORFV played roles in the regulation of key factors relevant to apoptosis, autoimmunity/inflammation, angiogenesis, and the cell cycle. Finally, data was presented to validate that ORFV infection induces oncolytic activity by enhancing apoptosis in vivo and in vitro. In conclusion, ORFV could be an oncolytic virus for CRC therapy.Long non‑coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4‑AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4‑AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4‑AS1 were explored in MCL clinical samples. The effects of FOXP4‑AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK‑8, crystal violet and Transwell assays. The downstream molecules of FOXP4‑AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4‑AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4‑AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4‑AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4‑AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4‑AS1 was found to act as a competing endogenous (ce)RNA for miR‑423‑5p to regulate the expression of nucleus accumbens‑associated 1 (NACC1). The negative regulation of FOXP4‑AS1 on miR‑423‑5p compared to that of miR‑423‑5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4‑AS1 and miR‑423‑5p, and that between miR‑423‑5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR‑423‑5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4‑AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4‑AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR‑423‑5p. FOXP4‑AS1 may serve as a novel therapeutic target for patients with MCL.Ovarian cancer is a gynecological malignancy with high mortality. Adjuvant therapy such as chemoradiotherapy inevitably leads to side effects and drug resistance. In recent years, traditional Chinese medicine has been widely studied for its safety, effectiveness, and unique pharmacological effects. Polyphyllin VII is an important component of Rhizoma paridis saponins, and has cytotoxic effects on many types of cancer cells. The aim of the present study was to evaluate the anti‑tumor activity of polyphyllin VII in human ovarian cancer cells. Recent studies found that polyphyllin VII induces mitochondrial pathway apoptosis by increasing mitochondrial division, but the specific mechanism was unclear. The results of this study revealed that polyphyllin VII could effectively induce mitochondrial dysfunction, including increased mitochondrial division and reactive oxygen species (ROS) production. check details Notably, the mitochondrial location of dynamin‑related protein 1 (DRP1) plays an important role in its function. In addition, polyphyllin VII enhanced the mitochondrial localization of DRP1 which is mediated by increased protein phosphatase 2A (PP2A) activity, and decreased AKT activity. A specific PP2A inhibitor, LB100, attenuated mitochondrial division and apoptosis in cells caused by polyphyllin VII, confirming the function of the PP2A/AKT pathway in polyphyllin VII treatment. Additionally, xenotransplantation experiments have also confirmed the anti‑tumor effect of polyphyllin VII in vivo. Therefore, interference of the mitochondrial translocation of DRP1 through PP2A/AKT pathway may be an attractive and effective therapeutic approach by polyphyllin VII in ovarian cancer. This may provide new strategies for polyphyllin VII in the clinical treatment of ovarian cancer.Rho family GTPase 3 (RND3) is involved in multiple physiological activities involving the Rho kinase‑dependent signaling pathway. The present study revealed a novel role of RND3 in the regulation of apoptosis in the brain. Using immunofluorescence and TUNEL assays, a decreased rate of brain apoptosis was observed in Rnd3‑knockout mice. In addition, the function of RND3 in promoting apoptosis was determined in PC12 cells by immunoblotting assays and flow cytometry analysis in RNA interference and overexpression experiments. Furthermore, the present study demonstrated that Rnd3 and P65 protein interacted using immunoprecipitation analysis, and Rnd3 regulated apoptosis via its association with NF‑κB P65. Notably, Rnd3 blocked the anti‑apoptotic action of NF‑κB P65 in vitro by downregulating P65. Therefore, RND3‑NF‑κB P65 represents a novel signaling pathway in the regulation of brain apoptosis. The present study suggested an alternative approach for the treatment of neurodegenerative diseases through regulation of apoptosis via the RND3‑NF‑κB P65 signaling pathway in the central nervous system.Epidermal growth factor receptor (EGFR) is overexpressed in various tumors and is associated with cancer initiation, progression, and poor prognosis. Despite the achievements made by tyrosine kinase inhibitors and monoclonal antibodies in certain cases, many patients have not benefited from such treatment due to resistance. Immunotoxins (ITs) are antibody‑cytotoxin chimeric molecules with specific cell killing ability, which have achieved different degrees of success in the treatment of a wide range of cancers in clinical trials. The aim of the current study was to examine a novel targeting EGFR recombinant immunotoxin Bs/cucurmosin (CUS) generated by fusing CUS to the EGFR‑specific nanobody 7D12‑9G8. Bs/CUS was successfully expressed in Escherichia coli strain BL21 (DE3) in a soluble form. Furthermore, it retained binding capacity and specificity with EGFR and was superior to rE/CUS, a monospecific IT we reported previously. In vitro results showed that Bs/CUS could be internalized into the cytoplasm and selectively kill cells in the picomolar range. Flow cytometry showed that Bs/CUS killed the cells mediated by the apoptosis pathway. Taken together, results of the current study indicated that Bs/CUS is a promising candidate that should be further evaluated as a cancer therapeutic for the treatment of EGFR‑positive tumors.Novel quinazolinone compounds have been studied in the field of drug discovery for a long time. Among their broad range of pharmacological effects, certain compounds effectively inhibit cancer cell proliferation. MJ‑33 is a quinazolinone derivative with proposed anticancer activities that was synthesized in our laboratory. The present study aimed to evaluate the anticancer activity of MJ‑33 in fluorouracil (5FU)‑resistant colorectal cancer cells (HT‑29/5FUR) and to investigate the underlying molecular mechanisms. The cell viability assay results indicated that HT‑29/5FUR cell viability was inhibited by MJ‑33 treatment in a concentration‑dependent manner compared with the control group. The cellular morphological alterations observed following MJ‑33 treatment indicated the occurrence of apoptosis and autophagy, as well as inhibition of cell proliferation in a time‑dependent manner compared with the control group. The acridine orange, LysoTracker Red and LC3‑green fluorescent protein staining results indicated that MJ‑33 treatment significantly induced autophagy compared with the control group.
My Website: https://www.selleckchem.com/products/gmx1778-chs828.html
Studies have shown that suppression of both the JAK/STAT3 pathway and epithelial‑mesenchymal transition (EMT) may overturn the resistance of non‑small cell lung cancer (NSCLC) cells to gefitinib. Zoledronic acid (ZA) injection is used to treat and prevent multiple forms of osteoporosis, hypercalcemia and bone metastasis‑related complications of malignancy. Clinical research has shown that ZA may exert antitumour effects and delay the progression of NSCLC. In the present study, we investigated whether ZA combined with gefitinib could re‑sensitise NSCLC cells to gefitinib in vitro and in vivo through inhibition of the JAK/STAT3 signalling pathway and EMT reversal. The results revealed that ZA potently increased the sensitivity of gefitinib‑resistant lung cancer cells to gefitinib. ZA decreased activation of JAK/STAT3 signalling and reversed EMT in the H1975 and HCC827GR cell lines. Furthermore, addition of IL‑6 to ZA‑pretreated gefitinib‑resistant cell lines abrogated the effect of ZA and restored the cellular resistance to tyrosine kinase inhibitors. Finally, ZA‑based combinatorial therapy effectively inhibited the growth of xenografts derived from gefitinib‑resistant cancer cells, which was correlated with the inhibition of the JAK/STAT3 signalling pathway and EMT reversal. In conclusion, ZA re‑sensitised gefitinib‑resistant lung cancer cells through inhibition of the JAK/STAT3 signalling pathway and EMT reversal. The combination of ZA and gefitinib may be a promising therapeutic strategy to reverse gefitinib resistance and prolong the survival of patients with NSCLC.Following the publication of the above article, the authors have realized that Fig. 5A was published with certain errors; essentially, the authors needed to perform further experiments to validate certain of their results, and the Blank and si‑NC control data in Fig. 5A were included from an incorrect set of experiments (the intended si‑NUSAP1 experimental data from the flow cytometric analyses, however, were presented correctly in the published Figure). The corrected version of Fig. 5, featuring the panels for the Blank and si‑NC control data in Fig. 5A from the same set of experiments, is shown opposite. The authors have confirmed that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum. Furthermore, they apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Oncology Reports 36 1506-1516, 2016; DOI 10.3892/or.2016.4955].Orf virus (ORFV) is a favorable oncolytic viral carrier in research, and ORFV strain NZ2 has been revealed to have antitumor effects in animal models mediated by immunoregulation profile. However, the antitumor effects triggered by the ORFV in colorectal cancer (CRC) cells is poorly characterized. The in vivo and in vitro roles of ORFV in CRC were determined using western blotting, colony formation, CCK‑8, wound scratch assay, qPCR, and animal models. Furthermore, cytokine antibody chip assay, flow cytometry, western blotting, and immunohistochemical (IHC) assays were conducted to explore the potential mechanism of ORFV. The present data revealed that ORFV strain NA1/11 infected and inhibited the in vitro growth and migration of CRC cells. By establishing a CRC model in Balb/c mice, it was revealed that ORFV strain NA1/11 significantly inhibited the in vivo growth and migration of CRC cells. A cytokine antibody array was utilized to obtain a more comprehensive profile revealing the differentially expressed cytokines in ORFV infection. Cytokines, such as IL‑7, IL‑13, IL‑15, CD27, CD30, pentraxin 3, and B lymphocyte chemoattractant (BLC), were upregulated. Axl, CXCL16, ANG‑3, MMP10, IFN‑γ R1 and VEGF‑B were downregulated. The results indicated that ORFV played roles in the regulation of key factors relevant to apoptosis, autoimmunity/inflammation, angiogenesis, and the cell cycle. Finally, data was presented to validate that ORFV infection induces oncolytic activity by enhancing apoptosis in vivo and in vitro. In conclusion, ORFV could be an oncolytic virus for CRC therapy.Long non‑coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4‑AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4‑AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4‑AS1 were explored in MCL clinical samples. The effects of FOXP4‑AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK‑8, crystal violet and Transwell assays. The downstream molecules of FOXP4‑AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4‑AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4‑AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4‑AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4‑AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4‑AS1 was found to act as a competing endogenous (ce)RNA for miR‑423‑5p to regulate the expression of nucleus accumbens‑associated 1 (NACC1). The negative regulation of FOXP4‑AS1 on miR‑423‑5p compared to that of miR‑423‑5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4‑AS1 and miR‑423‑5p, and that between miR‑423‑5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR‑423‑5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4‑AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4‑AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR‑423‑5p. FOXP4‑AS1 may serve as a novel therapeutic target for patients with MCL.Ovarian cancer is a gynecological malignancy with high mortality. Adjuvant therapy such as chemoradiotherapy inevitably leads to side effects and drug resistance. In recent years, traditional Chinese medicine has been widely studied for its safety, effectiveness, and unique pharmacological effects. Polyphyllin VII is an important component of Rhizoma paridis saponins, and has cytotoxic effects on many types of cancer cells. The aim of the present study was to evaluate the anti‑tumor activity of polyphyllin VII in human ovarian cancer cells. Recent studies found that polyphyllin VII induces mitochondrial pathway apoptosis by increasing mitochondrial division, but the specific mechanism was unclear. The results of this study revealed that polyphyllin VII could effectively induce mitochondrial dysfunction, including increased mitochondrial division and reactive oxygen species (ROS) production. check details Notably, the mitochondrial location of dynamin‑related protein 1 (DRP1) plays an important role in its function. In addition, polyphyllin VII enhanced the mitochondrial localization of DRP1 which is mediated by increased protein phosphatase 2A (PP2A) activity, and decreased AKT activity. A specific PP2A inhibitor, LB100, attenuated mitochondrial division and apoptosis in cells caused by polyphyllin VII, confirming the function of the PP2A/AKT pathway in polyphyllin VII treatment. Additionally, xenotransplantation experiments have also confirmed the anti‑tumor effect of polyphyllin VII in vivo. Therefore, interference of the mitochondrial translocation of DRP1 through PP2A/AKT pathway may be an attractive and effective therapeutic approach by polyphyllin VII in ovarian cancer. This may provide new strategies for polyphyllin VII in the clinical treatment of ovarian cancer.Rho family GTPase 3 (RND3) is involved in multiple physiological activities involving the Rho kinase‑dependent signaling pathway. The present study revealed a novel role of RND3 in the regulation of apoptosis in the brain. Using immunofluorescence and TUNEL assays, a decreased rate of brain apoptosis was observed in Rnd3‑knockout mice. In addition, the function of RND3 in promoting apoptosis was determined in PC12 cells by immunoblotting assays and flow cytometry analysis in RNA interference and overexpression experiments. Furthermore, the present study demonstrated that Rnd3 and P65 protein interacted using immunoprecipitation analysis, and Rnd3 regulated apoptosis via its association with NF‑κB P65. Notably, Rnd3 blocked the anti‑apoptotic action of NF‑κB P65 in vitro by downregulating P65. Therefore, RND3‑NF‑κB P65 represents a novel signaling pathway in the regulation of brain apoptosis. The present study suggested an alternative approach for the treatment of neurodegenerative diseases through regulation of apoptosis via the RND3‑NF‑κB P65 signaling pathway in the central nervous system.Epidermal growth factor receptor (EGFR) is overexpressed in various tumors and is associated with cancer initiation, progression, and poor prognosis. Despite the achievements made by tyrosine kinase inhibitors and monoclonal antibodies in certain cases, many patients have not benefited from such treatment due to resistance. Immunotoxins (ITs) are antibody‑cytotoxin chimeric molecules with specific cell killing ability, which have achieved different degrees of success in the treatment of a wide range of cancers in clinical trials. The aim of the current study was to examine a novel targeting EGFR recombinant immunotoxin Bs/cucurmosin (CUS) generated by fusing CUS to the EGFR‑specific nanobody 7D12‑9G8. Bs/CUS was successfully expressed in Escherichia coli strain BL21 (DE3) in a soluble form. Furthermore, it retained binding capacity and specificity with EGFR and was superior to rE/CUS, a monospecific IT we reported previously. In vitro results showed that Bs/CUS could be internalized into the cytoplasm and selectively kill cells in the picomolar range. Flow cytometry showed that Bs/CUS killed the cells mediated by the apoptosis pathway. Taken together, results of the current study indicated that Bs/CUS is a promising candidate that should be further evaluated as a cancer therapeutic for the treatment of EGFR‑positive tumors.Novel quinazolinone compounds have been studied in the field of drug discovery for a long time. Among their broad range of pharmacological effects, certain compounds effectively inhibit cancer cell proliferation. MJ‑33 is a quinazolinone derivative with proposed anticancer activities that was synthesized in our laboratory. The present study aimed to evaluate the anticancer activity of MJ‑33 in fluorouracil (5FU)‑resistant colorectal cancer cells (HT‑29/5FUR) and to investigate the underlying molecular mechanisms. The cell viability assay results indicated that HT‑29/5FUR cell viability was inhibited by MJ‑33 treatment in a concentration‑dependent manner compared with the control group. The cellular morphological alterations observed following MJ‑33 treatment indicated the occurrence of apoptosis and autophagy, as well as inhibition of cell proliferation in a time‑dependent manner compared with the control group. The acridine orange, LysoTracker Red and LC3‑green fluorescent protein staining results indicated that MJ‑33 treatment significantly induced autophagy compared with the control group.
My Website: https://www.selleckchem.com/products/gmx1778-chs828.html
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