Establishment and characterization of a KIT‐positive and stem cell factor‐producing cell line, KTHOS, derived from human osteosarcoma

Hitora, Toshiaki; Yamamoto, Toshiyuki; Akisue, Toshihiro; Marui, Takashi; Nakatani, Tetsuya; Kawamoto, Teruya; Nagira, Keiko; Yoshiya, Shinichi; Kurosaka, Masahiro

doi:10.1111/j.1440-1827.2005.01787.x

Cited by 8 publications

(5 citation statements)

References 20 publications

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“…The most striking finding is the presence of distinct subpopulations in both HDP and HGF that co‐express the ligand and its receptor (Fig 4A,B). Co‐expression of SCF and c‐kit has been reported in osteosarcoma cells (31), where an autocrine loop promoting cell proliferation was proposed. Our cells do not show evidence of any neoplastic transformation, therefore the possible role of any autocrine signaling requires further study.…”

Section: Discussionmentioning

confidence: 99%

Expression of stem cell factor and its receptor, c‐kit, in human oral mesenchymal cells

Gagari

Rand

Tayari

et al. 2006

European J Oral Sciences

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Stem cell factor (SCF) is the pleiotropic ligand for the tyrosine kinase receptor, c-kit. Ligand and receptor are usually expressed in different cell types, and binding of SCF to c-kit promotes cell proliferation, differentiation, and recruitment of progenitor cells in various biologic systems. However, the localization of these two molecules in cells of the oral cavity has not been systematically examined. We investigated the expression of SCF and c-kit in human dental pulp (HDP) cells as well as in human gingival fibroblasts (HGF). Both alternatively spliced isoforms of SCF were detected (through reverse transcription-polymerase chain reaction) in RNA obtained from the two cell types. Western analysis established that both cell types express SCF and/or c-kit, whereas flow cytometry demonstrated distinct cell populations expressing only the ligand (SCF), only the receptor (c-kit), or co-expressing the two. HDP cultures showed higher soluble SCF (sSCF) production associated with faster cell growth, as compared with HGF cultures. In both cell types, however, sSCF levels appeared to increase as a result of in vitro aging and/or differentiation.

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Section: Discussionmentioning

confidence: 99%

Expression of stem cell factor and its receptor, c‐kit, in human oral mesenchymal cells

Gagari

Rand

Tayari

et al. 2006

European J Oral Sciences

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“…Tumor types that have been shown to simultaneously express c-Kit and its ligand include breast carcinomas, colorectal carcinomas, small cell lung carcinoma (SCLC), gynecological tumors and neuroblastomas (reviewed in [83]). Recently, a osteosarcoma cell line established from a primary osteosarcoma lesion in the distal femur was shown to express both SCF and c-Kit, indicating the presence of an autocrine loop [84]. Malignant mesothelioma is often resistant to chemotherapy.…”

Section: Autocrine Loops Of C-kit and Scfmentioning

confidence: 99%

The Stem Cell Factor Receptor/c-Kit as a Drug Target in Cancer

Lennartsson¹,

Rönnstrand

2006

CCDT

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Tyrosine phosphorylation has a key role in intracellular signaling. Inappropriate proliferation and survival cues in tumor cells often occur as a consequence of unregulated tyrosine kinase activity. Much of the current development of anti-cancer therapies tries to target causative proteins in a specific manner to minimize side-effects. One attractive group of target proteins is the kinases. c-Kit is a receptor tyrosine kinase that normally controls the function of primitive hematopoietic cells, melanocytes and germ cells. It has become clear that uncontrolled activity of c-Kit contributes to formation of an array of human tumors. The unregulated activity of c-Kit may be due to overexpression, autocrine loops or mutational activation. This makes c-Kit an excellent target for cancer therapies in these tumors. In this review we will highlight the current knowledge on the signal transduction molecules and pathways activated by c-Kit under normal conditions and in cancer cells, and the role of aberrant c-Kit signaling in cancer progression. Recent advances in the development of specific inhibitors interfering with these signal transduction pathways will be discussed.

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“…KTHOS and TNMY-1 were previously established at our laboratory 49,50 . The Nara-H cell line was obtained from ScienStuff Co. (Nara, Japan) 51 .…”

Section: Methodsmentioning

confidence: 99%

“…Four human sarcoma cell lines, two osteosarcoma cell lines (KTHOS and MG-63) and two MFH cell lines (Nara-H and TNMY-1) and a normal human knee chondrocyte cell line (NHAC-kn) were used in in vitro studies. KTHOS and TNMY-1 were previously established at our laboratory 49 , 50 . The Nara-H cell line was obtained from ScienStuff Co. (Nara, Japan) 51 .…”

Section: Methodsmentioning

confidence: 99%

Regulation of Mitochondrial Proliferation by PGC-1α Induces Cellular Apoptosis in Musculoskeletal Malignancies

Onishi

Ueha

Kawamoto

et al. 2014

Sci Rep

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A number of studies have reported that decreased mitochondrial numbers are linked with neoplastic transformation and/or tumor progression, including resistance to apoptosis. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1a) is a multi-functional transcriptional coactivator that regulates the activities of multiple nuclear receptors and transcriptional factors involved in mitochondrial biogenesis. In this study, we observed that the number of mitochondria in sarcoma tissues, such as osteosarcoma and malignant fibrous histiocytoma, is significantly lower than that in normal muscle tissue or benign tumors, and that increasing the number of mitochondria by PGC-1a overexpression induces mitochondrial apoptosis in human sarcoma cell lines. The findings suggest that decreased mitochondrial numbers may contribute to musculoskeletal tumor progression, and that regulation of mitochondrial numbers by PGC-1a could be a potent therapeutic tool for human malignancies.M usculoskeletal malignancies are clinically aggressive and have high metastatic behavior in various organs. Although many chemotherapeutic protocols are used for human sarcomas, the current chemotherapeutic strategies for high-grade sarcomas have been ineffective, and the prognoses of patients can be extremely poor because of local recurrence and distant metastases 1 . Therefore, new therapeutic strategies against high-grade sarcomas need to be established. We have previously reported several therapeutic strategies against high-grade sarcomas [2][3][4] . Mitochondria are cytoplasmic organelles that play essential roles in cellular energy metabolism and programmed cell death 5 . Although the majority of mitochondrial proteins are synthesized by nuclear DNA (nDNA), mitochondria possess their own genome, called mitochondrial DNA (mtDNA) 6 . Thousands of mitochondria are found in each cell, and the number of mitochondria per cell is known to vary with cell or tissue origin, and to change under different internal or external microenvironments, such as hypoxia, and stimulation by steroid hormones 7,8 . Quantitative changes in mitochondrial numbers have been observed in many cancers as a decrease in hepatocellular carcinoma, renal cell carcinoma, advanced gastric cancer and breast cancer [9][10][11][12][13][14] , or an increase in head and neck cancers, ovarian cancer, and esophageal squamous cell carcinoma [15][16][17]

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Establishment and characterization of a KIT‐positive and stem cell factor‐producing cell line, KTHOS, derived from human osteosarcoma

Cited by 8 publications

References 20 publications

Expression of stem cell factor and its receptor, c‐kit, in human oral mesenchymal cells

Expression of stem cell factor and its receptor, c‐kit, in human oral mesenchymal cells

The Stem Cell Factor Receptor/c-Kit as a Drug Target in Cancer

Regulation of Mitochondrial Proliferation by PGC-1α Induces Cellular Apoptosis in Musculoskeletal Malignancies

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