Genetic and biological characterization of human myeloma cell lines: An overwiew of the lines established at Kawasaki Medical School

Otsuki, Takemi; Yata, Kenichiro; Nakazawa, Naozo; Sakaguchi, Haruko; Yawata, Yoshihito; Ueki, Ayako

doi:10.1002/1438-826x(200005)1:1<48::aid-gnfd48>3.0.co;2-b

Cited by 12 publications

(13 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[19][20][21] The cells were maintained in RPMI 1640 (Lonza). The culture medium was supplemented with 10% fetal bovine serum (Lonza) and 1% Antibiotic-Antimycotic solution (Invitrogen) in a 5% CO 2 incubator.…”

Section: Cell Culturementioning

confidence: 99%

Mitochondrial modulation decreases the bortezomib-resistance in multiple myeloma cells

et al. 2013

View full text Add to dashboard Cite

Multiple myeloma (MM) is an incurable hematological malignancy that causes most patients to eventually relapse and die from their disease. The 20S proteasome inhibitor bortezomib has emerged as an effective drug for MM treatment; however, intrinsic and acquired resistance to bortezomib has already been observed in MM patients. We evaluated the involvement of mitochondria in resistance to bortezomib-induced cell death in two different MM cell lines (bortezomib-resistant KMS20 cells and bortezomib-sensitive KMS28BM cells). Indices of mitochondrial function, including membrane potential, oxygen consumption rate and adenosine-5 0 -triphosphate and mitochondrial Ca 21 concentrations, were positively correlated with drug resistance of KMS cell lines. Mitochondrial genes including CYPD, SOD2 and MCU were differentially expressed in KMS cells. Thus, changes in the expression of these genes lead to changes in mitochondrial activity and in bortezomib susceptibility or resistance, and their combined effect contributes to differential sensitivity or resistance of MM cells to bortezomib. In support of this finding, coadministration of bortezomib and 2-methoxyestradiol, a SOD inhibitor, rendered KMS20 cells sensitive to apoptosis. Our results provide new insight into therapeutic modalities for MM patients. Studying mitochondrial activity and specific mitochondrial gene expression in fresh MM specimens might help predict resistance to proapoptotic chemotherapies and inform clinical decision-making.

show abstract

Section: Cell Culturementioning

confidence: 99%

Mitochondrial modulation decreases the bortezomib-resistance in multiple myeloma cells

et al. 2013

View full text Add to dashboard Cite

show abstract

“…33 So far, only 57 cases of PE have been reported, 4 of them included in this study. In our system, BM and PE myeloma cells were highly related, since they had been generated from the same individuals (KMS12 and KMS21).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, BM and PE belonged to the same clone, since KMS12BM and KMS12PE shared the same karyotypic abnormality, and the KMS21BM and KMS21PE had the same immunoglobulin (Ig) production. 33 …”

Section: Introductionmentioning

confidence: 99%

“…KMS12BM and KMS12PE were established from a single patient, as were KMS21BM and KMS21PE. KMS cells were established in vitro as described 33,34 ; to avoid in vitro selection, all KMS cell lines were studied within the third/fifth in vitro culture passage. The cells were grown in RPMI 1640 (Invitrogen, Milan, Italy) supplemented with 10% fetal bovine serum (FBS; Invitrogen) at 37°C in a humidified atmosphere with 5% CO 2 .…”

mentioning

confidence: 99%

See 1 more Smart Citation

HLA class I, NKG2D, and natural cytotoxicity receptors regulate multiple myeloma cell recognition by natural killer cells

Carbone

Neri

Mesuraca

et al. 2005

Blood

292

278

View full text Add to dashboard Cite

IntroductionNatural killer (NK) cells are cytotoxic and cytokine-producing lymphocytes, involved in the immune defense against viral infections and tumors. 1 Their homeostasis is regulated by cytokines and membrane associate receptors able to inhibit or activate cellular programs. 2 The inhibitory receptors are well characterized and described extensively in several reviews. [3][4][5] Triggering of NK cells depends largely on NK receptor member D of the lectinlike receptor family (NKG2D) and natural cytotoxicity receptors (NCRs): NKp46, NKp44, NKp30. 6,7 NCRs are involved in the recognition of several tumor cell lines, although their ligands remain elusive. 6 NKG2D recognizes the MHC (major histocompatibility complex) class I chain-related (MIC) protein A (MICA) and B (MICB); both are nonclassic class I molecules. The UL16-binding proteins (ULBP1-3 or RAET1 proteins; ULBP1-3 in this paper) are the second group of NKG2D ligands in humans. MICs are expressed during virus infection or cell transformation; ULBP expression in fresh tumor cells is essentially unknown; only long-term cultured in vitro cell lines have been looked at so far. [8][9][10] Cytotoxic T lymphocytes (CTLs) and interferons (IFNs) have a key role in tumor progression and tumor "immune-editing process." 11 MHC class I molecule loss is a frequent event in tumor progression and could prevent CTL recognition. However, theoretically, NK cells could recognize MHC class I-defective tumors, according with the "missing self hypothesis." 12 So far, only in mouse models NK cells were demonstrated to destroy in vivo lymphoma and melanoma tumors with reduced MHC class I expression and/or with high levels of activating target structures. [13][14][15] Even though almost 30 years ago human NK cells were discovered for their in vitro antitumor cytotoxicity, we still have little information concerning the regulation of their antitumor activity in vivo or ex vivo. 16,17 Therefore, several questions remain to be addressed to understand the antineoplastic potential of human NK lymphocytes:1. HLA class I molecules are reported to be down-regulated during solid tumor progression. 18 19,20 Other hematopoietic-derived cells can stimulate NK lymphocytes as described for dendritic cells (DCs). 21 The B-cell membrane-associated proteins CD40 and CD1 regulate natural killer cell cytotoxicity. [22][23][24][25] Furthermore, NK lymphocytes are specifically activated after bone marrow graft but not by other tissue transplantations. 26 They localize in lymph nodes and spleen, mainly in B-cell follicles and in the marginal zone. 27 Blood, spleen, and bone marrow are the anatomic districts where the highest number and activity of NK cells are present. 1 Taking together these considerations, hematologic malignancies (B-cell-derived tumors in particular) could be considered an appealing system to investigate the potential role of NK cells in the control of tumor progression.Multiple myeloma (MM) is a plasma cell-derived tumor. It is characterized by accumulation of plasma cells in th...

show abstract

“…The samples for the cell line control were made using cDNAs from various human myeloma cell lines established at the Kawasaki Medical School such as KMM-1 having a translocation of c-myc and CCND3, KMS-12Pe and BM having a CCND1 translocation and KMS-11 with the FGFR3 translocation (27)(28)(29)(30)(31)(32). In addition, cDNA from each cell line was subjected to MP-RT-PCR and ensured that the cell linespecific overexpressed genes were amplified (data not shown).…”

Section: Mp-rt-pcr For the Detection Of Major Overexpressed Genes In mentioning

confidence: 99%

Quick detection of overexpressed genes caused by myeloma-specific chromosomal translocations using multiplex RT-PCR

et al. 2011

View full text Add to dashboard Cite

Abstract. Multiple myeloma (MM) is a malignancy of the plasmocyte and is associated with various symptoms such as anemia, immunodeficiency, bone lesions and kidney insufficiency. Although prognosis was poor until some years ago, recent advances that introduced newer molecular targeting agents such as bortezomib and thalidomide have resulted in a better prognosis for MM. However, clinical manifestations and the relationship between cellular and molecular findings, including chromosomal translocation and the related overexpression of oncogenes such as ccNd1 (cyclin d1) and FGFR3 (fibroblast growth factor receptor 3), remain unclear. It has been reported that a specific translocation may influence the prognosis of MM. Although translocations and overexpressed genes should be examined in ordinary clinical investigations, limited definitive assays for translocation involve the use of FISH (fluorescent in situ hybridization) or SKY (special karyotypic) methods. We therefore, attempted to establish a quick detection method for major translocated genes such as FGFR3, ccNd1, ccNd3 and MAF using multiplex RT-PcR (MP-RT-PCR). MP-RT-PCR can be performed within several to 24 h after bone marrow samples are taken. Two of 21 bone marrow blood samples from MM patients were analyzed using MP-RT-PCR and double-color FISH, and the results of both methods were compatible. Future utilization and elaboration of this method may help our understanding of the cell biology and clinical features of MM.

show abstract

Genetic and biological characterization of human myeloma cell lines: An overwiew of the lines established at Kawasaki Medical School

Cited by 12 publications

References 12 publications

Mitochondrial modulation decreases the bortezomib-resistance in multiple myeloma cells

Mitochondrial modulation decreases the bortezomib-resistance in multiple myeloma cells

HLA class I, NKG2D, and natural cytotoxicity receptors regulate multiple myeloma cell recognition by natural killer cells

Quick detection of overexpressed genes caused by myeloma-specific chromosomal translocations using multiplex RT-PCR

Contact Info

Product

Resources

About