Monday, 13 March 2017

MCF-7 (tế bào gây ung thư vú)

MCF-7 - tế bào gây ung thư vú

From Wikipedia, the free encyclopedia

MCF-7 Cells
MCF-7 is a breast cancer cell line isolated in 1970 from a 69-year-old Caucasian woman. MCF-7 is the acronym of Michigan Cancer Foundation-7, referring to the institute in Detroit where the cell line was established in 1973 by Herbert Soule and co-workers.[1] The Michigan Cancer Foundation is now known as the Barbara Ann Karmanos Cancer Institute.[2]
Prior to MCF-7, it was not possible for cancer researchers to obtain a mammary cell line that was capable of living longer than a few months.[3]
The patient, Frances Mallon died in 1970. Her cells were the source of much of current knowledge about breast cancer.[1][4] At the time of sampling, she was a nun in the convent of Immaculate Heart of Mary in Monroe, Michigan under the name of Sister Catherine Frances.
MCF-7 and two other breast cancer cell lines, named T-47D and MDA-MB-231, account for more than two-thirds of all abstracts reporting studies on mentioned breast cancer cell lines, as concluded from a Medline-based survey.[5]

Characteristics of MCF-7 cells[edit]

The characteristics of MCF-7 cells are:[1][4][5][6][7][8]
This cell line retained several characteristics of differentiated mammary epithelium, including the ability to process estradiol via cytoplasmic estrogen receptors and the capability of forming domes.
Tumor necrosis factor alpha (TNF alpha) inhibits the growth of MCF-7 breast cancer cells. Treatment with anti-estrogens can modulate the secretion of insulin-like growth factor binding proteins.
PIK3CA helical mutations were identified in MCF-7, but with low AKT activation.[9]

MCF-7


MCF-7 est le nom de la lignée de cellules tumorales mammaires la plus utilisée dans les laboratoires de recherche sur le cancer du sein. Ainsi, elle est mentionnée dans plus d'un tiers des articles scientifiques rapportant des travaux sur des lignées tumorales mammaires (voir PubMed). Avec deux autres lignées courantes, appelées T-47D et MDA-MB-231, elle représente les deux-tiers de ces articles1. MCF-7 est l'acronyme de Michigan Cancer Foundation - 7, en référence à l'institut de Detroit où la lignée fut établie -au septième essai-, en 1973, par Herbert Soule et collègues2.
La lignée MCF-7 a été établie en culture in vitro à partir d'un épanchement pleural prélevé chez une patiente de 69 ans atteinte d'un cancer du sein métastatique. Cette patiente, dont le nom est ignoré de l'immense majorité des chercheurs en cancérologie, est décédée en 1970. Ses cellules ont été à l'origine d'une bonne partie des connaissances actuelles sur le cancer du sein2,3. Elle s'appelait Frances Mallon, et était à l'époque du prélèvement religieuse au couvent du Cœur Immaculé de Marie (Immaculate Heart of Mary Convent, Monroe, Michigan), sous le nom de sœur Catherine Frances.

Caractéristiques de la lignée[modifier | modifier le code]

  • Tumeur primaire : canalaire invasive
  • Origine des cellules : épanchement pleural
  • Présence de récepteurs d'œstrogènes : oui
  • Réponse proliférative aux œstrogènes : oui
  • Présence de récepteurs de progestérone : oui
  • Amplification du gène ERBB2 (Her2/neu) : non
  • Mutation dans le gène TP53, codant la protéine p53 : non ("type sauvage")
  • Tumorigénicité chez la souris : oui, moyennant supplémentation en œstrogènes
  • Catégorie de phénotype : luminal épithélial
Sur base des références1,2,3,4,5,6.
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DU145 (tế bào gây ung thư tuyến tiền liệt)

DU145- tế bào gây ung thư tuyến tiền liệt

From Wikipedia, the free encyclopedia
DU145 (DU-145) and PC3 human prostate cancer cell lines are the "classical" cell lines of prostatic cancer.[1] DU145 cells have moderate metastatic potential compared to PC3 cells which have high metastatic potential.[2]
The DU145 cell line was derived from brain metastasis.[3] DU145 are not hormone-sensitive and do not express prostate-specific antigen (PSA).
It has been demonstrated that administration of NFkappaB ligand RANKL promoted DU145 cell invasion in bone, resulting in osteolytic lesions. DU145 cells also produce soluble factors that activate pre-osteoblast precursors and increase RANKL expression, thus facilitating prostate cancer metastasis in bone.[4]
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LNCaP (tế bào gây ung thư tuyến tiền liệt)

LNCaP- tế bào gây ung thư tuyến tiền liệt

From Wikipedia, the free encyclopedia

Properties of common PCa cell lines
LNCaP cells are a cell line of human cells commonly used in the field of oncology. LNCaP cells are androgen-sensitive human prostate adenocarcinoma cells derived from the left supraclavicular lymph node metastasis from a 50-year-old caucasian male in 1977. They are adherent epithelial cells growing in aggregates and as single cells.[1]
One major obstacle to the conducting the most clinically relevant prostate cancer (PCa) research has been the lack of cell lines that closely mimic human disease progression. Two hallmarks of metastatic human prostate cancer include the shift of aggressive PCa from androgen-sensitivity to an Androgen Insensitive (AI) state, and the propensity of PCa to metastasize to bone. Although the generation of AI cell lines has been quite successful as demonstrated in the “classic” cell lines DU145 and PC3, the behavior of these cells in bone does not fully mimic clinical human disease. It is well established that human PCa bone metastasis form osteoblastic lesions rather than osteolytic lesions seen in other cancers like breast cancer.[2][3] Similarly, PC-3 and DU145 cells form osteolytic tumors. To develop an AI-PCa cell model that more closely mimics clinical disease, LNCaP sublines have been generated to provide the most clinically relevant tissue culture tools to date.

History[edit]

The LNCaP cell line was established from a metastatic lesion of human prostatic adenocarcinoma. The LNCaP cells grow readily in vitro (up to 8 x 105 cells/sq cm; doubling time, 60 hr), form clones and are highly resistant to human fibroblast interferon.[1] LNCaP cells have a modal chromosome number of 76 to 91, indicative of a human male karyotype with several marker chromosomes[1] The malignant properties of LNCaP cells are maintained in athymic nude mice which develop tumors at the injection site and show a similar doubling time in vivo.[1]
High-affinity specific androgen and estrogen receptors are present in the cytosol and nuclear fractions.[1] The LNCaP line is hormonally responsive, shown by in vitro 5 alpha-dihydrotestosterone modulation of cell growth and acid phosphatase production.[1] LNCaP cells also express Prostate Specific Antigen (PSA).[1] In vivo, Male mice develop tumors earlier and at a greater frequency than do females and hormonal manipulations show that the frequency of tumor development correlates with serum androgen levels.[1] The rate of the tumor growth, however, is independent of the gender or hormonal status of the host.[1]

C4/C5 and C4-2[edit]

Wu et al. (1994) reproduced the human-derived LNCaP tumors in immunocompromised mice by co-injection of LNCaP cells with MS human bone fibroblasts.[4] Cells were subcutaneously injected at multiple sites into the mouse flank and after approximately 4 weeks of growth, tumors were easily detectable by physical examination and had a high rate of growth (17-33 mm3/day).[4]
To replicate the hallmark shift of PCa cells to AI, LNCaP host mice were castrated by way of midscrotal incision at approximately 8 weeks post injection. Tumors were maintained in castrated hosts for 4 to 5 weeks at which time remaining tumors were harvested. In total, two subsets of cells were collected from castrated hosts: C4 and C5, collected at 4 and 5 weeks respectively.[4]
To further select for AI-PCa cells, the C4 subline was co-injected with MS human fibroblasts into a castrated host. The resulting tumors were isolated and an additional subline was generated, C4-2.[4]
Karyotype comparisons indicate that LNCaP cells grown in intact hosts (M subline) have a modal chromosomal distribution number of 83, C4 and C5 sublines with 85, and the C4-2 subline with 83.[4]
To further verify that these cells were of human origin karyotype analysis determined that the parental LNCaP cells had 7 distinct marker chromosomes, with two copies of each. The M, C4, C5, and C4-2 sublines contained most of the marker chromosomes, with the M subline being most similar to the parental LNCaP cells. C4,C5 and C4-2 are only minutely distinct from LNCaP and the M subline with the addition of a marker chromosome resulting from a segment addition to chromosome 6. A Y chromosome is not present in most C4, C5 and C4-2 cells, suggesting major chromosomal alterations.[4]
C4,C5, and C4-2 sublines grow well under identical tissue culture conditions as LNCaP with similar growth rates. Parental LNCaP, M, C4, and C5 subline have similar baseline gene expression levels of ornithine decarboxylase (ODC) and Prostate Specific Antigen (PSA) however, M, C4, and C5 sublines express 5-10X more PSA mRNA. M, C4, C5 and C4-2 also expressed reduced human androgen receptor mRNA as expected in AI cells.[4]
Androgen Insensitivity All sublines were treated with dihydrotestosterone (DHT), a high-affinity ligand for AR. DHT treatment elicited markedly reduced growth in C4 and C5 cells and no growth in C4-2 cells when compared to the high rate of growth seen in LNCaP cells, suggesting reduced androgen sensitivity in C4 and C5 and AI in C4-2 cells. Whole-cell AR assay also indicated that LNCaP cells have a much higher affinity form of AR (Kd = 159 pM) when compared to C4-2 (Kd = 267 pM).[4]
Tumorigenicity C4 and C5 sublines exhibit greatly increased tumorigenicity when injected in intact male mice, unlike parental LNCaP cells. C4 and C5 were also able to form highly vascularized carcinomas in castrated mice when co-injected with MS human fibroblasts. The C4-2 subline more readily forms tumors in intact hosts than C4 and C5 sublines and they are the only cells able to form tumors in castrated host without co-injection with MS human bone fibroblasts. These same C4-2 tumors stained for PSA and secreted high levels of PSA into the growth medium.[4]

C4-2B[edit]

To generate a bone metastatic subline, C4-2 cells were orthotopically injected into castrated male mice. These cells formed large primary tumors of the prostate, lymph nodes, as well as osseus tumors. Isolation of these osseus tumors resulted in the C4-2B subline. C4-2B cells were positive for PSA and cytokeratin 8, confirming their prostatic origin. Most importantly, immunohistochemical staining of the C4-2B tumors were positive for osteoblast activity suggesting the induction of osteoblastic tumor formation mirroring the progression of human PCa.[5]
When cultured in a “promineralization medium” that contains ascorbic acid (known to promote skeletal-like ECM formation in osteoblasts) and a source of phosphate (for hydroxyapatite formation), C4-2B cells produce and retain approximately 8x more mineralized calcium than parental LNCaP cells. C4-2B cells also express higher levels of osteoprotegerin (OPG), alkaline phosphatase, bone sialoprotein (BSP), Osteocalcin (OCN), RANKL, and Osteonectin (OSN) mRNA, all of which are highly expressed by osteoblasts. Osteoblast promoter activity is also higher in C4-2B cells when compared to LNCaP, as indicated by Cbfa1 transcription factor expression. Concomitantly, BMP7, a known inducer of Cbfa1, is also more highly expressed in C4-2B cells, further suggesting many osteoblast-like properties.[3]
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A549 (tế bào adenocarcinomic nhân phế nang đấy biểu mô)

A549 cell-tế bào adenocarcinomic nhân phế nang đấy biểu mô


A549 cells under DIC microscopy, from a 3-4 days old culture, showing an abundance of intercellular connections, including possible cytonemes, filopodia and other epithelial bridges. (These cells have endocytosed 25x73 nm colloidal gold nanorods.)
A549 cells are adenocarcinomic human alveolar basal epithelial cells. The A549 cell line was first developed in 1972 by D. J. Giard, et al. through the removal and culturing of cancerous lung tissue in the explanted tumor of a 58-year-old caucasian male.[1][2] In nature, these cells are squamous and responsible for the diffusion of some substances, such as water and electrolytes, across the alveoli of lungs. If A549 cells are cultured in vitro, they grow as monolayer cells, adherent or attaching to the culture flask.[1] The human alveolar epithelial cell line A549 may be anchored or suspended in a solution in vitro.
Another characteristic of these cells is that they are able to synthesize lecithin and contain high level of unsaturated fatty acids, which are important to maintain the membrane phospholipids in cells.[1] A549 cell line are widely used as an in vitro model for a type II pulmonary epithelial cell model for drug metabolism and as a transfection host.[3][4]
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Hep G2 (tế bào gây ung thư gan)

Hep G2- tế bào gây ung thư gan

From Wikipedia, the free encyclopedia

Hep G2 Cells
Hep G2 is a human liver cancer cell line.
Hep G2 is a perpetual cell line which was derived from the liver tissue of a 15-year-old Caucasian American male with a well-differentiated hepatocellular carcinoma. These cells are epithelial in morphology, have a modal chromosome number of 55, and are not tumorigenic in nude mice.[1] The cells secrete a variety of major plasma proteins, e.g., albumin, transferrin, and the acute-phase proteins fibrinogen, alpha 2-macroglobulin, alpha 1-antitrypsin, transferrin, and plasminogen.[citation needed] They have been grown successfully in large-scale cultivation systems. Hepatitis B virus surface antigens have not been detected. HepG2 will respond to stimulation with human growth hormone.[citation needed]
HepG2 cells are a suitable in vitro model system for the study of polarized human hepatocytes. (Another well-characterized polarized hepatocyte cell line is the rat hepatoma-derived hybrid cell line WIF-B[2]). With the proper culture conditions, HepG2 cells display robust morphological and functional differentiation with a controllable formation of apical and basolateral cell surface domains (van IJzendoorn et al., 1997; 2000, etc.) that resemble the bile canalicular (BC) and sinusoidal domains, respectively, in vivo.
Because of their high degree of morphological and functional differentiation in vitro, HepG2 cells are a suitable model to study the intracellular trafficking and dynamics of bile canalicular and sinusoidal membrane proteins and lipids in human hepatocytes in vitro.[citation needed] This can be important for the study of human liver diseases that are caused by an incorrect subcellular distribution of cell surface proteins, e.g., hepatocanalicular transport defects such as Dubin-Johnson Syndrome and progressive familial intrahepatic cholestasis (PFIC), and familial hypercholesterolemia.[citation needed] HepG2 cells and their derivatives are also used as a model system for studies of liver metabolism and toxicity of xenobiotics[citation needed], the detection of environmental and dietary cytotoxic and genotoxic (and thus cytoprotective, anti-genotoxic, and cogenotoxic) agents,[3] understanding hepatocarcinogenesis[citation needed], and for drug targeting studies[citation needed]. HepG2 cells are also employed in trials with bio-artificial liver devices[citation needed].
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