共查询到20条相似文献,搜索用时 31 毫秒
1.
Laura L. Worth Shu-Fang Jia Taeha An Eugenie S. Kleinerman 《Cancer immunology, immunotherapy : CII》1999,48(6):312-320
ImmTher, a liposome-encapsulated lipophilic disaccharide tripeptide derivative of muramyl dipeptide, previously showed activity
against liver and lung colorectal metastases in a phase I trial. The purpose of the current studies was to investigate whether
ImmTher could up-regulate specific cytokine gene expression and protein production, as well as activate the tumoricidal or
cytostatic activity of human monocytes. ImmTher induced the expression and production of interleukin(IL)-1α IL-1β, IL-6, IL-8,
IL-12, macrophage chemotactic and activating factor, and tumor necrosis factor α but not IL-2 or IL-10. Cytostatic or cytotoxic
monocyte activity was stimulated against human Ewing's sarcoma, osteosarcoma, and melanoma cells but not breast cancer cells.
Production and secretion of these cytokine proteins may play a role in the antitumor activity of ImmTher.
Received: 15 December 1998 / Accepted: 18 March 1999 相似文献
2.
Hirofumi Shoda Keishi Fujio Yumi Yamaguchi Akiko Okamoto Tetsuji Sawada Yuta Kochi Kazuhiko Yamamoto 《Arthritis research & therapy》2007,8(6):R166
IL-32 is a newly described cytokine in the human found to be an in vitro inducer of tumor necrosis factor alpha (TNFα). We examined the in vivo relationship between IL-32 and TNFα, and the pathologic role of IL-32 in the TNFα-related diseases – arthritis and colitis.
We demonstrated by quantitative PCR assay that IL-32 mRNA was expressed in the lymphoid tissues, and in stimulated peripheral
T cells, monocytes, and B cells. Activated T cells were important for IL-32 mRNA expression in monocytes and B cells. Interestingly,
TNFα reciprocally induced IL-32 mRNA expression in T cells, monocyte-derived dendritic cells, and synovial fibroblasts. Moreover,
IL-32 mRNA expression was prominent in the synovial tissues of rheumatoid arthritis patients, especially in synovial-infiltrated
lymphocytes by in situ hybridization. To examine the in vivo relationship of IL-32 and TNFα, we prepared an overexpression model mouse of human IL-32β (BM-hIL-32) by bone marrow transplantation.
Splenocytes of BM-hIL-32 mice showed increased expression and secretion of TNFα, IL-1β, and IL-6 especially in response to
lipopolysaccharide stimulation. Moreover, serum TNFα concentration showed a clear increase in BM-hIL-32 mice. Cell-sorting
analysis of splenocytes showed that the expression of TNFα was increased in resting F4/80+ macrophages, and the expression of TNFα, IL-1β and IL-6 was increased in lipopolysaccharide-stimulated F4/80+ macrophages and CD11c+ dendritic cells. In fact, BM-hIL-32 mice showed exacerbation of collagen-antibody-induced arthritis and trinitrobenzen sulfonic
acid-induced colitis. In addition, the transfer of hIL-32β-producing CD4+ T cells significantly exacerbated collagen-induced arthritis, and a TNFα blockade cancelled the exacerbating effects of hIL-32β.
We therefore conclude that IL-32 is closely associated with TNFα, and contributes to the exacerbation of TNFα-related inflammatory
arthritis and colitis. 相似文献
3.
Roman Paduch Martyna Kandefer-Szerszeń 《In vitro cellular & developmental biology. Animal》2009,45(9):543-550
Colon adenocarcinoma is one of the most common fatal malignancies in Western countries. Progression of this cancer is dependent
on tumor microenvironmental signaling molecules such as transforming growth factor-β (TGF-β) or acetylcholine (ACh). The present
study was conducted to assess the influence of recombinant human transforming growth factor (rhTGF)-β1 or ACh on nitric oxide
(NO) and interleukin-1β (IL-1β) secretion by three human colon adenocarcinoma cell lines: HT29, LS180, and SW948, derived
from different grade tumors (Duke’s stage). The cells were cultured in 2D and 3D (spheroids) conditions. Colon carcinoma cells
exhibited different sensitivities to rhTGF-β1 or ACh dependent on the tumor grade and the culture model. ACh exhibited significant
inhibitory effects towards NO, endothelial nitric oxide synthase (eNOS), and IL-1β secretion especially by tumor cells derived
form Duke’s C stage of colon carcinoma. rhTGF-β1 also decreased NO, IL-1β, and eNOS expression, but its effect was lower than
that observed after the administration of ACh. The inhibition of NO and IL-1β production was more striking in 3D tumor spheroids
than in 2D culture monolayers. Taken together, the TGF-β1–ACh axis may regulate colon carcinoma progression and metastasis
by altering NO secretion and influence inflammatory responses by modulating IL-1β production. 相似文献
4.
Olle Björkdahl Anette Gjörloff Wingren Gunnar Hedlund Lennart Ohlsson M. Dohlsten 《Cancer immunology, immunotherapy : CII》1997,44(5):273-281
Interleukin(IL)-1 differs from most other cytokines in its lack of a signal sequence. This results in intracellular retention
of the immature proform. The release of IL-1 has been shown to be restricted predominantly to activated monocytes and macrophages
and to be associated with apoptosis of the producer cell. These features have limited the investigation of IL-1 in early immune
responses. In order to study the biological effects of local IL-1β release during an antitumour immune response, we used B16
mouse melanoma cells transduced with mature human IL-1β cDNA constructs. To obtain a released form of human IL-1β (ssIL-1β),
the signal sequence from the related IL-1 receptor antagonist was ligated to the cDNA that encoded the mature form of IL-1β.
When cells of the poorly immunogenic B16 melanoma cell line were transduced with IL-1β by retroviral infection, high levels
of the protein were detected intracellularly, whereas cells transduced with IL-1β containing the signal sequence secreted
most of their protein. The in vitro growth of the melanoma cells was unaffected by the IL-1β or ssIL-1β gene transfer. In
contrast, the in vivo subcutaneous tumour growth of the ssIL-1β-transduced B16 cells in syngeneic C57BL/6 mice was significantly
reduced compared with the IL-1β- and the mock-transduced controls. Immunohistochemical analysis revealed the infiltration
of macrophages to be strong in B16/ssIL-1β, moderate in B16/IL-1β and minimal in control tumours. Furthermore, a moderate
infiltration of CD4+ cells and of scattered dendritic cells was detected in B16/ssIL-1β tumours whereas very few or no CD4+ cells and dendritic cells were seen in the B16/IL-1β or control tumours. Following in vivo growth, all the tumours up-regulated
ICAM-1 on their cell surfaces. However, the percentage of ICAM-1-expressing cells was two- to fourfold higher in B16/ssIL-1β
tumours compared to the control. The data suggest that IL-1β acts in vivo, either directly or indirectly, as a chemotactic
factor for monocytes, T helper cells and dendritic cells. This supports IL-1β having a regulatory effect on tumour growth
when locally released in the tumour area.
Received: 12 November 1996 / Accepted: 6 May 1997 相似文献
5.
Interleukin-1 directly regulates hormone-dependent human breast cancer cell proliferation in vitro 总被引:1,自引:0,他引:1
Direct in vitro effects of IL-1 on hormone-dependent (MCF-7 and ZR-75-B) and independent (HS-578-T and MDA-231) human breast cancer cell proliferation were investigated in short-term and long-term cell cultures. For short-term (48 h) studies [3H]thymidine uptake was used as an index of proliferation, while for long-term (12 day) cultures actual cell numbers were determined. Initial studies, conducted with MCF-7 cells, demonstrated that both forms of recombinant human IL-1 (alpha and beta) at 10(-11) M inhibited [3H]thymidine uptake by MCF-7 by 70%, and by day 7 of the long-term study alpha and beta IL-1 at 10(-11) M inhibited MCF-7 cell growth by 80%. IL-1, while inhibiting the growth of another hormone-dependent breast cancer cell line; ZR-75-B, had no effect on the hormone-independent cell lines MDA-231 and HS-578-T. The differing proliferative responses of the hormone-dependent and independent cells to IL-1 may, in part, be due to the expression of IL-1 receptors on these cells, in that MCF-7 cells express IL-1 receptors [dissociation constant (Kd) = 2.0 x 10(-10) M; receptor density = 2,500 sites per cell and mol wt = 80,000] while the hormone-independent MDA-231 cells do not. 相似文献
6.
7.
Association of increased basement membrane invasiveness with absence of estrogen receptor and expression of vimentin in human breast cancer cell lines. 总被引:31,自引:0,他引:31
E W Thompson S Paik N Brünner C L Sommers G Zugmaier R Clarke T B Shima J Torri S Donahue M E Lippman 《Journal of cellular physiology》1992,150(3):534-544
Lack of estrogen receptor (ER) and presence of vimentin (VIM) associate with poor prognosis in human breast cancer. We have explored the relationships between ER, VIM, and invasiveness in human breast cancer cell lines. In the matrigel outgrowth assay, ER+/VIM- (MCF-7, T47D, ZR-75-1), and ER-/VIM- (MDA-MB-468, SK-Br-3) cell lines were uninvasive, while ER-/VIM+ (BT549, MDA-MB-231, MDA-MB-435, MDA-MB-436, Hs578T) lines formed invasive, penetrating colonies. Similarly, ER-/VIM+ cell lines were significantly more invasive than either the ER+/VIM- or ER-/VIM- cell lines in the Boyden chamber chemoinvasion assay. Invasive activity in nude mice was only seen with ER-/VIM+ cell lines MDA-MB-231, MDA-MB-435 and MDA-MB-436. Hs578T cells (ER-/VIM+) showed hematogenous dissemination to the lungs in one of five mice, but lacked local invasion. The ER-/VIM+ MCF-7ADR subline was significantly more active than the MCF-7 cells in vitro, but resembled the wild-type MCF-7 parent in in vivo activity. Data from these cell lines suggest that human breast cancer progression results first in the loss of ER, and subsequently in VIM acquisition, the latter being associated with increased metastatic potential through enhanced invasiveness. The MCF-7ADR data provide evidence that this transition can occur in human breast cancer cells. Vimentin expression may provide useful insights into mechanisms of invasion and/or breast cancer cell progression. 相似文献
8.
Two human leukemia cells K562 and THP-1, the breast cancer lines MCF-7 and ZR-75-1, and the melanoma line MDA-MB-435S were
compared by flowcytometry for their behaviour at increasing levels of 3BP. K562 and THP-1 responded to 3BP by membrane depolarization
and increased ROS; MCF-7 and ZR-75-1 showed decreased polarization and low ROS increase; MDA-MB-435S had limited depolarization
and no ROS increase. THP-1 cells exposed to a range of 3BP concentrations in combination with DCA showed increase of polarization,
slight ROS increase, and weakened nuclear integrity. 3BP and DCA show no synergism, but have complementary destructive effects
on THP-1 cells. The data led to the conclusion that the THP-1 cells do not carry a functional membrane monocarboxylate transporter
(MCT) or that 3BP circumvents MCT binding and can enter these cells independently. 相似文献
9.
Pérez E García-Martínez O Arroyo-Morales M Reyes-Botella C Ruiz C 《Bioscience reports》2006,26(4):281-289
Background/Aims Recent reports demonstrated that osteoblast-like cells can also exert activities directly associated with the immune system (cytokine synthesis, antigen presentation, phagocytosis and stimulation of T lymphocytes). The present study aimed to analyze the effect of Transforming growth factorβ1 (TGFβ1), Fibroblast growth factor basic (FGFb), Platelet-derived growth factor-BB (PDGF-BB), Interleukin-1β (IL-1β), Interleukin-2 (IL-2), Lipopolysaccharide (LPS) and Interferon-γ (IFNγ) on the expression on osteoblast-like cells of antigens involved in antigen presentation.Methods Flow cytometry was used to investigate whether the growth factors FGFb, TGFβ1, PDGF-BB, IL-2, IL-1β, LPS and IFNγ modulate the expression on cultured human osteoblast-like cells of different antigens involved in antigen-presentation and T cell activation.Results TGFβ1 treatment significantly reduced the expression of CD54 and CD86. IL-1β treatment significantly enhanced the expression of CD54, CD86 and HLA-DR. LPS and IFNγ treatments produced a major increase in CD54, CD80, CD86 and HLA-DR expression. Expression of these antigen-presenting molecules was not significantly modified by FGFb, PDGF-BB or IL-2 treatment. 相似文献
10.
Masami Ogasawara David A. Sirbasku 《In vitro cellular & developmental biology. Plant》1988,24(9):911-920
Summary Growth of the MCF-7, T47D, and ZR-75-1 human breast cancer cells was established in a serum-free defined medium (MOM-1) composed
of a 1∶1 (vol/vol) mixture of Ham's F12 medium and Dulbecco's modified Eagle's medium containing 15 mM HEPES (pH 7.2), 2 mM 1-glutamine, 20 μg/ml glutathione, 10 μg/ml insulin, 10 μg/ml transferrin (Tf), 10 ng/ml selenous acid, 0.3 nM triiodothyronine, 50 μg/ml ethanolamine, 20 ng/ml epidermal, growth factor, 2.0 nM 17β-estradiol, and 1.0 mg/ml bovine serum albumin (BSA). Proliferation in MOM-1 was 50 to 70% of the serum stimulated rate.
Deletion of components from MOM-1 gave a medium (Tf-BSA) containing only HEPES, 10 μg/ml Tf, and 200 μg/ml BSA, which sustained
MCF-7 and T47D cells in a slowly dividing and mitogen responsive state; ZR-75-1 cells required Tf plus 1.0 mg/ml BSA. In Tf-BSA,
insulin and insulin-like growth factor I(IGF-I) were mitogenic with ED50 values of 2 to 3 ng/ml and 30 to 150 pg/ml, respectively, with MCF-7 cells. The T47D cells were responsive to these factors
in Tf-BSA but required 10-fold higher concentrations for ED50. At saturating concentrations, insulin and IGF-I promoted 1.5 to 3.5 cell population doublings over controls in 8 d. At≤ng/ml
concentrations, epidermal growth factor, insulin-like growth factor II, and basic fibroblast growth factor were mitogenic
for human breast cancer cells in Tf-BSA. Mitogen activities in uterus and pituitary extracts were assayed readily in Tf-BSA.
This new method offers a convenient means of comparing the potencies of growth-promoting factors on human breast cancer cells
without interfering activities known to be present in serum.
This work was supported by grants CA-38024 and CA-26617, from the National Cancer Institute, Bethesda, MD, and by American
Cancer Society grant BC-255 and grant 2225 from the Council for Tobacco Research, USA, Inc. 相似文献
11.
R Blumenthal W McLaughlin J Jordan E Cryan W Bloomer 《Biochemical and biophysical research communications》1987,149(2):642-648
Cultures of the human mammary carcinoma line ZR-75-1 secrete a growth inhibitory factor (GIF) that, when diluted, slows the growth of MDA-MB-231 and MCF-7 cells. Undiluted "conditioned" media prevents cell division from occurring in both human breast cancer lines. ZR-75-1 cells are unaffected by this factor. The amount of GIF in the culture media is related to the confluency of the ZR-75-1 cells. The activity of this GIF is not altered by DNAse or RNAse but is destroyed by heating or trypsin. Growth inhibition is 85-90% reversible if conditioned media is replaced with fresh media. 相似文献
12.
Danielle Burger 《Arthritis research & therapy》2000,2(6):472-5
The intricate interactions that regulate relationships between endogenous tissue cells and infiltrating immune cells in the rheumatic joint, particularly in rheumatoid arthritis (RA), were the subject of the meeting. A better understanding of these interactions might help to define intervention points that could be used to develop specific therapies. The presentations and discussions highlighted the fact that, once chronic inflammation is established, several pro-inflammatory loops involving tumour necrosis factor (TNF)-α and interleukin (IL)-1β can be defined. Direct cellular contact with stimulated T lymphocytes induces TNF-α and IL-1β in monocytes which in turn induce functions in fibroblast-like synoviocytes. The latter include the production of stromal cell-derived factor-1α (SDF-1α) which enhances the expression of CD40L in T cells, which stimulates SDF-1α production in synoviocytes, which in turn protects T and B cells from apoptosis and enhances cell recruitment thus favoring inflammatory processes. IL-1β and TNF-α also induce IL-15 in fibroblast-like synoviocytes, which induces the production of IL-17 which in turn potentiates IL-1β and TNF-α production in monocyte-macrophages. This underlines the importance of TNF-α and IL-1β in RA pathogenesis, and helps explain the efficiency of agents blocking the activity of these cytokines in RA. Factors able to block the induction of cytokine production (such as apolipoprotein A-I [apo A-I] and interferon [IFN]-β) might interfere more distally in the inflammatory process. Furthermore, stimulated T lymphocytes produce osteoclast differentiation factor (ODF), which triggers erosive functions of osteoclasts. Therefore, factors capable of affecting the level of T lymphocyte activation, such as IFN-β, IL-15 antagonist, or SDF-1α antagonist, might be of interest in RA therapy. 相似文献
13.
It has been reported that estrogen receptor-positive MCF-7 cells express TauT, a Na+-dependent taurine transporter. However, there is a paucity of information relating to the characteristics of taurine transport
in this human breast cancer cell line. Therefore, we have examined the characteristics and regulation of taurine uptake by
MCF-7 cells. Taurine uptake by MCF-7 cells showed an absolute dependence upon extracellular Na+. Although taurine uptake was reduced in Cl- free medium a significant portion of taurine uptake persisted in the presence of NO3
-. Taurine uptake by MCF-7 cells was inhibited by extracellular β-alanine but not by L-alanine or L-leucine. 17β-estadiol increased
taurine uptake by MCF-7 cells: the Vmax of influx was increased without affecting the Km. The effect of 17β-estradiol on taurine uptake by MCF-7 cells was dependent upon the presence of extracellular Na+. In contrast, 17β-estradiol had no significant effect on the kinetic parameters of taurine uptake by estrogen receptor-negative
MDA-MB-231 cells. It appears that estrogen regulates taurine uptake by MCF-7 cells via TauT. In addition, Na+-dependent taurine uptake may not be strictly dependent upon extracellular Cl-. 相似文献
14.
Kazuhide Takahashi 《BMC cell biology》2001,2(1):23-10
Background
Structural requirements for the β1 integrin functions in cell adhesion, spreading and signaling have been well documented mainly for fibroblasts. In this study, we examined the reason for the reduced surface expression of β1 integrin in human breast cancer MCF-7 cells compared to normal human breast epithelial (HBE) cells, both of which adhered to collagen type IV. 相似文献15.
Localization of thymosin β10 in breast cancer cells: relationship to actin cytoskeletal remodeling and cell motility 总被引:1,自引:1,他引:0
Beta-thymosins are polypeptides involved in the regulation of actin polymerization and thymosin β10 and β4 have been implicated
in sequestration of monomeric (G-) actin. Additionally, experimental overexpression of thymosin β10 has been found to result
in increases in F-actin bundles as well as in cell motility and spreading. We have studied the distribution of endogenously
expressed thymosin β10 in cultured human breast cancer cell lines. Both unperturbed monolayer cultures and wound-healing models
were examined using double-staining for thymosin β10 and polymerized (F-) actin. Our findings show that thymosin β10 is expressed
in all three-cancer cell lines (SK-BR-3, MCF-7 and MDA-MB-231) studied. No or little staining was detected in confluent cells,
whereas strong staining occurred in semiconfluent cells and in cells populating monolayer wounds. Importantly, the distribution
of staining for thymosin β10 was inverse of staining for F-actin. These data support a physiological role for thymosin β10
in sequestration of G-actin as well as in cancer cell motility. 相似文献
16.
Expression of plasma membrane calcium pump isoform mRNAs in breast cancer cell lines 总被引:2,自引:0,他引:2
Lee WJ Roberts-Thomson SJ Holman NA May FJ Lehrbach GM Monteith GR 《Cellular signalling》2002,14(12):1015-1022
The plasma membrane Ca2+ ATPase (PMCA) is an important regulator of free intracellular calcium, with dynamic regulation in the rat mammary gland during lactation. Recent studies suggest that Ca2+ plays a role in cellular proliferation. To determine if PMCA expression is altered in tumorigenesis, we compared relative levels of PMCA1 mRNA. We found that the relative expression of PMCA1 mRNA is increased, by approximately 270% and 170%, in MCF-7 and MDA-MB-231 human breast cancer cell lines deprived of serum for 72 h, respectively, compared to the similarly treated MCF-10A human mammary gland epithelial cell line. Characterization of PMCA mRNA isoforms revealed that PMCA1b and PMCA4 mRNA are expressed in MCF-7, MDA-MB-231, SK-BR-3, ZR-75-1 and BT-483 breast cancer cell lines. We also detected PMCA2 mRNA expression in all the breast cancer cell lines examined. However, PMCA3 mRNA was only detected in BT-483 cells. Our results suggest that PMCA expression may be altered in breast cancer cell lines, suggesting altered Ca2+ regulation in these cell lines. Our results also indicate that breast cancer cell lines can express mRNAs for a variety PMCA isoforms. 相似文献
17.
Ceramide and glucosylceramide upregulate expression of the multidrug resistance gene MDR1 in cancer cells 总被引:2,自引:0,他引:2
Gouazé-Andersson V Yu JY Kreitenberg AJ Bielawska A Giuliano AE Cabot MC 《Biochimica et biophysica acta》2007,1771(12):1407-1417
In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp. Acute exposure (72 h) to C8-ceramide (5 microg/ml culture medium), a cell-permeable ceramide, increased MDR1 mRNA levels by 3- and 5-fold in T47D and in MDA-MB-435 cells, respectively. Acute exposure of MCF-7 and MDA-MB-231 cells to C8-GC (10 microg/ml culture medium), a cell-permeable analog of GC, increased MDR1 expression by 2- and 4- fold, respectively. Chronic exposure of MDA-MB-231 cells to C8-ceramide for extended periods enhanced MDR1 mRNA levels 45- and 390-fold at passages 12 and 22, respectively, and also elicited expression of P-gp. High-passage C8-ceramide-grown MDA-MB-231 (MDA-MB-231/C8cer) cells were more resistant to doxorubicin and paclitaxel. Incubation with [1-(14)C]C6-ceramide showed that cells converted short-chain ceramide into GC, lactosylceramide, and sphingomyelin. When challenged with 5 mug/ml [1-(14)C]C6-ceramide, MDA-MB-231, MDA-MB-435, MCF-7, and T47D cells took up 31, 17, 21, and 13%, respectively, and converted 82, 58, 62, and 58% of that to short-chain GC. Exposing cells to the GCS inhibitor, ethylenedioxy-P4, a substituted analog of 1-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol, prevented ceramide's enhancement of MDR1 expression. These experiments show that high levels of ceramide and GC enhance expression of the multidrug resistance phenotype in cancer cells. Therefore, ceramide's role as a messenger of cytotoxic response might be linked to the multidrug resistance pathway. 相似文献
18.
Summary The pathway of interleukin 1 (IL-1) secretion from the cell remains unclear. IL-1β is the major form produced by human monocytes,
and is synthesized as a precursor of 35kDa which is processed to the extracellular biologically active 17kDa form. We have
examined the intracellular localization of IL-1β in lipopolysaccharide (LPS)-stimulated human peripheral blood monocytes,
by immunocytochemistry and immunoprecipitation of subcellular fractions. LPS treatment slightly damaged the cells. Unstimulated
cells showed very little immunolabelling. In contrast, there was heavy immunolabelling on LPS stimulated cells. Immunolabelling
occured within the cytoplasm, nucleus and mitochondria. There was no immunolabelling on the membranous secretory organelles
and the plasma membrane. Blebs of cytoplasm budding from the cell surface were immunolabelled, suggesting an alternative route
of secretion of IL-1β from the cell. Immunoprecipitation studies confirmed these results. 相似文献
19.
20.
Various tumor cells express interleukin 7 (IL-7) and IL-7 variants. IL-7 has been confirmed to stimulate solid tumor cell proliferation. However, the effect of IL-7 variants on tumor cell proliferation remains unclear. In this study, we evaluated the role of IL-7δ5 (an IL-7 variant lacking exon 5) on proliferation and cell cycle progression of human MDA-MB-231 and MCF-7 breast cancer cells. The results showed that IL-7δ5 promoted cell proliferation and cell cycle progression from G1 phase to G2/M phase, associated with upregulation of cyclin D1 expression and the downregulation of p27(kip1) expression. Mechanistically, we found that IL-7δ5 induced the activation of Akt. Inhibition of PI3K/Akt pathway by LY294002 reversed the proliferation and cell cycle progression of MDA-MB-231 and MCF-7 cells induced by IL-7δ5. In conclusion, our findings demonstrate that IL-7δ5 variant induces human breast cancer cell proliferation and cell cycle progression via activation of PI3K/Akt pathway. Thus, IL-7δ5 may be a potential target for human breast cancer therapeutics intervention. 相似文献