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Natural killer cell lines in tumor immunotherapy

null

《医学前沿（英文）》 2012年 第6卷 第1期   页码 56-66 doi: 10.1007/s11684-012-0177-7

摘要：

Natural killer (NK) cells are considered to be critical players in anticancer immunity. However, cancers are able to develop mechanisms to escape NK cell attack or to induce defective NK cells. Current NK cell-based cancer immunotherapy is aimed at overcoming NK cell paralysis through several potential approaches, including activating autologous NK cells, expanding allogeneic NK cells, usage of stable allogeneic NK cell lines and genetically modifying fresh NK cells or NK cell lines. The stable allogeneic NK cell line approach is more practical for quality-control and large-scale production. Additionally, genetically modifying NK cell lines by increasing their expression of cytokines and engineering chimeric tumor antigen receptors could improve their specificity and cytotoxicity. In this review, NK cells in tumor immunotherapy are discussed, and a list of therapeutic NK cell lines currently undergoing preclinical and clinical trials of several kinds of tumors are reviewed.

关键词： natural killer cell     natural killer cell line     tumor immunotherapy     genetic modification    

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Correlativity study between expression of DNA double-strand break repair protein and radiosensitivity of tumor

Liang ZHUANG, Shiying YU, Xiaoyuan HUANG, Yang CAO, Huihua XIONG

《医学前沿（英文）》 2009年 第3卷 第1期   页码 26-29 doi: 10.1007/s11684-009-0008-7

摘要： DNA double-strand break (DSB) is generally regarded as the most lethal of all DNA lesions after radiation. Ku80, DNA-PK catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated (ATM) proteins are major DSB repair proteins. In this study, survival fraction at 2Gy (SF2) values of eight human tumor cell lines (including four human cervical carcinoma cell lines HeLa, SiHa, C33A, Caski, three human breast carcinoma cell lines MCF-7, MDA-MB-231, MDA-MB-453, and one human lung carcinoma cell line A549) were acquired by clone formation assay, and western blot was applied to detect the expressions of Ku80, DNA-PKcs and ATM protein. The correlativity of protein expression with SF2 value was analyzed by Pearson linear correlation analysis. We found that the expression of same protein in different cell lines and the expression of three proteins in the same cell line had a significant difference. The SF2 values were also different in eight tumor cell lines and there was a positive correlativity between the expression of DNA-PKcs and SF2 ( ＝0.723, = 0.043), but Ku80 and ATM expression had no correlation with SF2 ( >0.05). These findings suggest that the expression level of DNA-PKcs protein can be an indicator for predicting the radiosensitivity of tumor cells.

关键词： Ku80     DNA-PK(cs)-binding protein     human     ataxia telangiectasia mutated protein     tumor cell lines     radiosensitivity    

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Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

《医学前沿（英文）》 2008年 第2卷 第4期   页码 374-379 doi: 10.1007/s11684-008-0072-4

摘要： Expression of DNA methyltransferase 1 (DNMT1), which plays an important role on aberrantly methylated CpG in the promoter regions of tumor suppressor genes (TSGs), is higher in bladder cancer cells than in normal bladder cells. Therefore, its overexpression is closely related to tumor formation. In this study, the eukaryotic vector pshRNA-DNMT1 was constructed and transfected into T24 cells. Levels of DNMT1 mRNA and protein were detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Relative to the blank control at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1, the inhibitory rates of DNMT1 mRNA levels in T24 cells were 28.44%, 52.48%, 70.91%, respectively. Those of DNMT1 proteins were 24.27%, 57.79%, and 77.74%, respectively. Proliferation and apoptosis were assayed by MTT and flow cytometry with Annexin-V-FITC/PI staining. The growth inhibition rates of pshRNA-DNMT1 at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1 were (4.34 ± 0.76)%, (9.87 ± 1.54)% and (13.78 ± 1.93)%, respectively. There were statistically significant differences between pshRNA-DNMT1 and the control blank at each time points ( < 0.01); 24, 48 and 72 hours after T24 cells were transfected by pshRNA-DNMT1, the apoptosis rates of pshRNA-DNMT1 were (3.87 ± 0.81)%, (8.69 ± 1.23)% and (11.46 ± 1.24)%, respectively ( < 0.01 blank control). Based on this case, our conclusion is that the recombinant plasmid pshRNA-DNMT1 can silence the expression of gene DNMT1 mRNA and protein effectively, and to some extent, it also can inhibit the proliferation of bladder cancer cell and promote the cellular apoptosis.
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Immunosuppressive tumor microenvironment contributes to tumor progression in diffuse large B-cell lymphoma

《医学前沿（英文）》 2023年 第17卷 第4期   页码 699-713 doi: 10.1007/s11684-022-0972-8

摘要： Anti-CD19 chimeric antigen receptor (CAR)-T cell therapy has achieved 40%–50% long-term complete response in relapsed or refractory diffuse large B-cell lymphoma (DLBCL) patients. However, the underlying mechanism of alterations in the tumor microenvironments resulting in CAR-T cell therapy failure needs further investigation. A multi-center phase I/II trial of anti-CD19 CD28z CAR-T (FKC876, ChiCTR1800019661) was conducted. Among 22 evaluable DLBCL patients, seven achieved complete remission, 10 experienced partial remissions, while four had stable disease by day 29. Single-cell RNA sequencing results were obtained from core needle biopsy tumor samples collected from long-term complete remission and early-progressed patients, and compared at different stages of treatment. M2-subtype macrophages were significantly involved in both in vivo and in vitro anti-tumor functions of CAR-T cells, leading to CAR-T cell therapy failure and disease progression in DLBCL. Immunosuppressive tumor microenvironments persisted before CAR-T cell therapy, during both cell expansion and disease progression, which could not be altered by infiltrating CAR-T cells. Aberrant metabolism profile of M2-subtype macrophages and those of dysfunctional T cells also contributed to the immunosuppressive tumor microenvironments. Thus, our findings provided a clinical rationale for targeting tumor microenvironments and reprogramming immune cell metabolism as effective therapeutic strategies to prevent lymphoma relapse in future designs of CAR-T cell therapy.

关键词： anti-CD19 chimeric antigen receptor T     immunotherapy     diffuse large B cell lymphoma     tumor microenvironment     tumor-associated macrophage     metabolism    

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Gene expression disparity in giant cell tumor of bone

Xiaohua PAN, Shuhua YANG, Deming XIAO, Yong DAI, Lili REN

《医学前沿（英文）》 2009年 第3卷 第1期   页码 49-56 doi: 10.1007/s11684-009-0012-y

摘要： The aim of this paper was to study the differential gene expression of giant cell tumor of bone (GCTB) by gene chip technology. Total RNA of 8 fresh GCTB specimens (Jaffe I∶6 cases, II∶1 case, III∶1 case; Campanacci I∶6 cases, II∶1 case, III∶1 case; Enneking Staging G T M : 5 cases, G T M : 2 cases, G T M : 1 case) and 4 normal bony callus specimens (the control group) were extracted and purified to get mRNA and then reverse transcribed to complementary DNA, respectively. Microarray screening with a set of 8064 human cDNA genes was conducted to analyze the difference among the samples and the control. The hybridization signals were scanned. The gene expression disparity between the GCTB samples and normal bony callus was significantly different ( <0.01), and the disparity of over 5-fold was found in 47 genes in the GCTB specimens, with 25 genes up-regulated and 22 down-regulated including the extracellular matrix and transforming-related genes, oncogene and its homolog genes, cytokine and its receptor genes. Specific gene spectrum associated with GCTB can be identified by cDNA microarray, which will be the foundation of progressive etiology elucidation, diagnosis and treatment of GCTB.

关键词： giant cell tumor of bone     gene     microarray     cDNA    

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Microbiome subsets determine tumor prognosis and molecular characteristics of clear-cell renal cell carcinoma

《医学前沿（英文）》 doi: 10.1007/s11684-023-1029-3

摘要： Microbiome subsets determine tumor prognosis and molecular characteristics of clear-cell renal cell carcinoma: a multi-center integrated analysis of microbiome, metabolome, and transcriptome data

关键词： tumor prognosis molecular     Microbiome subsets determine     center analysis microbiome     transcriptome data    

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Identification of cancer stem cells provides novel tumor models for drug discovery

null

《医学前沿（英文）》 2012年 第6卷 第2期   页码 112-121 doi: 10.1007/s11684-012-0199-1

摘要：

Cancer stem cells (CSCs) have received considerable attention from the research community since they were first reported in human acute myeloid leukemia 15 years ago. Accumulating evidence suggests that CSCs are responsible for tumor initiation and progression, drug resistance, and metastasis in both liquid and solid tumors. These findings lead to the development of novel compounds targeting CSC populations that is becoming increasingly important for eradicating CSCs in heterogeneous tumor masses and to cure the cancer. Since 2003, we have participated in CSC studies and encountered crucial early events in the field. This article reviews the history of CSC biology, clarifies the term and its definition, and further addresses the issue of how to utilize CSCs in therapeutic target discovery and drug development based on our substantial experience.

关键词： cancer stem cell     tumor model     drug discovery    

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Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal

《医学前沿（英文）》 2022年 第16卷 第5期   页码 784-798 doi: 10.1007/s11684-021-0911-0

摘要： More than 85% of patients with uveal melanoma (UM) carry a GNAQ or GNA11 mutation at a hotspot codon (Q209) that encodes G protein α subunit q/11 polypeptides (Gαq/11). GNAQ/11 relies on palmitoylation for membrane association and signal transduction. Despite the palmitoylation of GNAQ/11 was discovered long before, its implication in UM remains unclear. Here, results of palmitoylation-targeted mutagenesis and chemical interference approaches revealed that the loss of GNAQ/11 palmitoylation substantially affected tumor cell proliferation and survival in UM cells. Palmitoylation inhibition through the mutation of palmitoylation sites suppressed GNAQ/11Q209L-induced malignant transformation in NIH3T3 cells. Importantly, the palmitoylation-deficient oncogenic GNAQ/11 failed to rescue the cell death initiated by the knock down of endogenous GNAQ/11 oncogenes in UM cells, which are much more dependent on Gαq/11 signaling for cell survival and proliferation than other melanoma cells without GNAQ/11 mutations. Furthermore, the palmitoylation inhibitor, 2-bromopalmitate, also specifically disrupted Gαq/11 downstream signaling by interfering with the MAPK pathway and BCL2 survival pathway in GNAQ/11-mutant UM cells and showed a notable synergistic effect when applied in combination with the BCL2 inhibitor, ABT-199, in vitro. The findings validate that GNAQ/11 palmitoylation plays a critical role in UM and may serve as a promising therapeutic target for GNAQ/11-driven UM.

关键词： uveal melanoma     mutant GNAQ/11     palmitoylation     BCL2     combination target therapy    

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Effect of atorvastatin on tumor growth and metastasis in a breast cancer cell xenograft model and its

Liu LIU MD, PhD, Yaogui NING MM, Chen CHEN MD, Daowen WANG MD, PhD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 443-446 doi: 10.1007/s11684-009-0079-5

摘要： This paper aims to evaluate the effects and the possible mechanisms of atorvastatin on tumor growth and metastasis in a xenograft tumor model. Twenty-four female athymic BALB/C mice with MDA-MB-435 xenograft tumors were randomly assigned to three groups: a control group, a low-dose atorvastatin treatment group, and a high-dose atorvastatin treatment group. The mice in the treatment groups began to be administered with atorvastatin (10 or 20 mg/kg per day) when the xenograft tumors reached 1 cm in diameter. At the end of the experiment, the tumor volume and weight and the lung metastasis colonies of each mouse were measured. Western blotting was applied to detect phosphorylation of protein kinase B (PKB, Akt), extracellular signal regulated kinase (ERK), c-Jun N-terminal Kinase (JNK), and the expression of cytochrome P450 (CYP) subtype CYP2J2. Atorvastatin suppressed xenograft tumor growth and metastasis both in the low-dose and the high-dose treatment groups ( < 0.05). Atorvastatin also decreased the phosphorylated Akt (p-Akt) and p-ERK but increased p-JNK expression. However, atorvastatin did not alter the expression of CYP2J2 in tumor tissue. This suggests that atorvastatin has the efficacy of suppressing tumor growth and metastasis . These effects were not dependent on down-regulation of CYP2J2 expression.

关键词： atorvastatin     xenograft tumor     metastasis     CYP2J2    

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Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cell

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

《医学前沿（英文）》 2010年 第4卷 第1期   页码 106-111 doi: 10.1007/s11684-010-0004-y

摘要： Hepatitis B virus X protein (HBx), a 17-kd protein encoded by X gene of hepatitis B virus (HBV), has been shown to function as a transcriptional trans-activator of a variety of viral and cellular promoter/enhancer elements. The aim of the study is to investigate the extracellular regulated protein kinases (ERKs) pathway of HBx on glomerular mesangial cell (GMC) proliferation and tumor necrosis factor-α (TNF-α) expression. The HBV X gene was amplified by polymerase chain reaction (PCR), inserted into the eukaryotic expression vector pCI-neo and confirmed by restriction endonuclease digestion and sequence analysis. PCI-neo containing HBV X gene (pCI-neo-X) was then transfected into cultured GMC line via liposome. GMC proliferation, TNF-α and its mRNA expression were compared in the condition of with or without U0126 in culture media. HBx, ERK and p-ERK expression in GMCs was assessed by Western blotting. TNF-α mRNA expression was assessed by semi-quantitative reverse transcription-PCR (RT-PCR). TNF-α level in supernatants was measured by ELISA. GMC proliferation was detected by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) kit. The results showed that HBx expression was found in transfected GMCs and became prominent at 36th and 48th h after transfection whether with or without U0126 in culture media. TNF-α mRNA expression was significantly decreased in U0126 group compared with U0126-free group. TNF-α levels in supernatants in PCI-neo-X transfection without U0126 group were (189.0±18.1) and (172.3±24.3) pg/mL at 36th and 48th h after transfection, respectively. In contrast, TNF-α levels in supernatants with U0126 were (65.6±11.6) and (84.0±24.6) pg/mL at 36th and 48th h, respectively. The TNF-α levels in the latter groups were significantly lower than those in the former groups (<0.05). GMCs proliferation was also lower in added U0126 group at 36th and 48th h after transfection. From above, we can conclude that HBx could induce GMC proliferation and increase TNF-α mRNA expression and its protein production. HBx upregulates TNF-α expression and induces cell proliferation of GMC line partly through ERK signal transduction pathway.

关键词： hepatitis B virus     X gene     glomerular mesangial cell line     extracellular regulated protein kinases     tumor necrosis factor-α    

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A survey on assembly lines and its types

Ullah SAIF,Zailin GUAN,Baoxi WANG,Jahanzeb MIRZA,Shiyang HUANG

《机械工程前沿（英文）》 2014年 第9卷 第2期   页码 95-105 doi: 10.1007/s11465-014-0302-1

摘要：

Assembly lines are useful for mass production of standard as well as customized products. Line balancing is an important issue, in this regard an optimal or near optimal balance can provide a fruitful savings in the initial cost and also in the running cost of such production systems. A survey of different problems in different types of assembly lines and some of the critical and on going research areas are highlighted here. The provided research information is momentous for the research community in assembly line area to proceed further in the presented issues of assembly lines.

关键词： assembly lines     line balancing     survey    

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Combined gemcitabine and CHK1 inhibitor treatment induces apoptosis resistance in cancer stem cell-likecells enriched with tumor spheroids from a non-small cell lung cancer cell line

null

《医学前沿（英文）》 2013年 第7卷 第4期   页码 462-476 doi: 10.1007/s11684-013-0270-6

摘要：

Evaluating the effects of novel drugs on appropriate tumor models has become crucial for developing more effective therapies that target highly tumorigenic and drug-resistant cancer stem cell (CSC) populations. In this study, we demonstrate that a subset of cancer cells with CSC properties may be enriched into tumor spheroids under stem cell conditions from a non-small cell lung cancer cell line. Treating these CSC-like cells with gemcitabine alone and a combination of gemcitabine and the novel CHK1 inhibitor PF-00477736 revealed that PF-00477736 enhances the anti-proliferative effect of gemcitabine against both the parental and the CSC-like cell populations. However, the CSC-like cells exhibited resistance to gemcitabine-induced apoptosis. Collectively, the spheroid-forming CSC-like cells may serve as a model system for understanding the mechanism underlying the drug resistance of CSCs and for guiding the development of better therapies that can inhibit tumor growth and eradicate CSCs.

关键词： drug resistance     cancer stem cell     checkpoint kinase 1 (CHK1)     PF-00477736     lung cancer     tumorigenicity    

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CAR T cells redirected against tumor-specific antigen glycoforms: can low-sugar antigens guarantee a

《医学前沿（英文）》 2022年 第16卷 第3期   页码 322-338 doi: 10.1007/s11684-021-0901-2

摘要： Immune-based therapies have experienced a pronounced breakthrough in the past decades as they acquired multiple US Food and Drug Administration (FDA) approvals for various indications. To date, six chimeric antigen receptor T cell (CAR-T) therapies have been permitted for the treatment of certain patients with relapsed/refractory hematologic malignancies. However, several clinical trials of solid tumor CAR-T therapies were prematurely terminated, or they reported life-threatening treatment-related damages to healthy tissues. The simultaneous expression of target antigens by healthy organs and tumor cells is partly responsible for such toxicities. Alongside targeting tumor-specific antigens, targeting the aberrantly glycosylated glycoforms of tumor-associated antigens can also minimize the off-tumor effects of CAR-T therapies. Tn, T, and sialyl-Tn antigens have been reported to be involved in tumor progression and metastasis, and their expression results from the dysregulation of a series of glycosyltransferases and the endoplasmic reticulum protein chaperone, Cosmc. Moreover, these glycoforms have been associated with various types of cancers, including prostate, breast, colon, gastric, and lung cancers. Here, we discuss how underglycosylated antigens emerge and then detail the latest advances in the development of CAR-T-based immunotherapies that target some of such antigens.

关键词： cancer immunotherapy     chimeric antigen receptor     solid tumors     tumor-associated antigen     glycosylation     O-glycans     adoptive cell therapy    

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Immunometabolism: a new dimension in immunotherapy resistance

《医学前沿（英文）》 2023年 第17卷 第4期   页码 585-616 doi: 10.1007/s11684-023-1012-z

摘要： Immune checkpoint inhibitors (ICIs) have demonstrated unparalleled clinical responses and revolutionized the paradigm of tumor treatment, while substantial patients remain unresponsive or develop resistance to ICIs as a single agent, which is traceable to cellular metabolic dysfunction. Although dysregulated metabolism has long been adjudged as a hallmark of tumor, it is now increasingly accepted that metabolic reprogramming is not exclusive to tumor cells but is also characteristic of immunocytes. Correspondingly, people used to pay more attention to the effect of tumor cell metabolism on immunocytes, but in practice immunocytes interact intimately with their own metabolic function in a way that has never been realized before during their activation and differentiation, which opens up a whole new frontier called immunometabolism. The metabolic intervention for tumor-infiltrating immunocytes could offer fresh opportunities to break the resistance and ameliorate existing ICI immunotherapy, whose crux might be to ascertain synergistic combinations of metabolic intervention with ICIs to reap synergic benefits and facilitate an adjusted anti-tumor immune response. Herein, we elaborate potential mechanisms underlying immunotherapy resistance from a novel dimension of metabolic reprogramming in diverse tumor-infiltrating immunocytes, and related metabolic intervention in the hope of offering a reference for targeting metabolic vulnerabilities to circumvent immunotherapeutic resistance.

关键词： immune cell     immunometabolism     metabolic reprogramming     immunotherapy     resistance     tumor microenvironment     immune checkpoint inhibitor    

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NADPH oxidase and reactive oxygen species as signaling molecules in carcinogenesis

Gang WANG

《医学前沿（英文）》 2009年 第3卷 第1期   页码 1-7 doi: 10.1007/s11684-009-0018-5

摘要： Reactive oxygen species (ROS) are small molecule metabolites of oxygen that are prone to participate in redox reactions their high reactivity. Intracellular ROS could be generated in reduced nicotinamide-adenine dinucleotidephosphate (NADPH) oxidase-dependent and/or NADPH oxidase-independent manners. Physiologically, ROS are involved in many signaling cascades that contribute to normal processes. One classical example is that ROS derived from the NADPH oxidase and released in neurotrophils are able to digest invading bacteria. Excessive ROS, however, contribute to pathogenesis of various human diseases including cancer, aging, dimentia and hypertension. As signaling messengers, ROS are able to oxidize many targets such as DNA, proteins and lipids, which may be linked with tumor growth, invasion or metastasis. The present review summarizes recent advances in our comprehensive understanding of ROS-linked signaling pathways in regulation of tumor growth, invasion and metastasis, and focuses on the role of the NADPH oxidase-derived ROS in cancer pathogenesis.

关键词： free radicals     tumor     phox     cell proliferation     cancer therapy    

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标题 作者 时间 类型 操作

Natural killer cell lines in tumor immunotherapy

null

期刊论文

Correlativity study between expression of DNA double-strand break repair protein and radiosensitivity of tumor

Liang ZHUANG, Shiying YU, Xiaoyuan HUANG, Yang CAO, Huihua XIONG

期刊论文

Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

期刊论文

Immunosuppressive tumor microenvironment contributes to tumor progression in diffuse large B-cell lymphoma

期刊论文

Gene expression disparity in giant cell tumor of bone

Xiaohua PAN, Shuhua YANG, Deming XIAO, Yong DAI, Lili REN

期刊论文

Microbiome subsets determine tumor prognosis and molecular characteristics of clear-cell renal cell carcinoma

期刊论文

Identification of cancer stem cells provides novel tumor models for drug discovery

null

期刊论文

Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal

期刊论文

Effect of atorvastatin on tumor growth and metastasis in a breast cancer cell xenograft model and its

Liu LIU MD, PhD, Yaogui NING MM, Chen CHEN MD, Daowen WANG MD, PhD,

期刊论文

Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cell

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

期刊论文

A survey on assembly lines and its types

Ullah SAIF,Zailin GUAN,Baoxi WANG,Jahanzeb MIRZA,Shiyang HUANG

期刊论文

Combined gemcitabine and CHK1 inhibitor treatment induces apoptosis resistance in cancer stem cell-likecells enriched with tumor spheroids from a non-small cell lung cancer cell line

null

期刊论文

CAR T cells redirected against tumor-specific antigen glycoforms: can low-sugar antigens guarantee a

期刊论文

Immunometabolism: a new dimension in immunotherapy resistance

期刊论文

NADPH oxidase and reactive oxygen species as signaling molecules in carcinogenesis

Gang WANG

期刊论文