Establishment of four pairs of canine mammary tumour cell lines derived from primary and metastatic origin and their E‐cadherin expression

Uyama, Rina; Nakagawa, Takayuki; Hong, Suk-In; Mochizuki, Manabu; Nishimura, Ryohei; Sasaki, Nobuo

doi:10.1111/j.1476-5810.2006.00098.x

Cited by 73 publications

(65 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CIP-p (primary origin) and CIP-m (metastatic origin) were previously generated from the same individual (Shih Tzu) 18 . CIP-p cells form small number of colonies in soft agar colony formation assay (data not shown), suggesting that CIP-p cells is likely to be a lower grade cancer than CIP-m.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The role of SET/I2PP2A in canine mammary tumors

Kake

Tsuji

Enjoji

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Canine mammary tumor is the most common neoplasm in female dogs, and it has generated considerable attention as a translational model for human breast cancer. Ser/Thr protein phosphatase 2A (PP2A) plays a critical role as a tumor suppressor, and SET/I2PP2A, the endogenous inhibitory protein of PP2A, binds directly to PP2A and suppresses its phosphatase activity. Here, we investigated the role of SET in the tumorigenic growth in canine mammary tumor as well as in the sensitivity of tumors to existing therapeutics. Elevated protein levels of SET were observed in advanced-stage of canine mammary tumor tissues of dogs compared with paired normal tissues. Knockdown of SET expression in a canine mammary tumor cell line CIP-m led to increased PP2A activity and decreased cell proliferation, colony formation, and in vivo tumor growth. We observed suppression of mTOR, β-catenin, and NFκB signaling by SET knockdown. The sensitivity of CIP-m cells to doxorubicin was decreased by SET knockdown, while SET knockdown in CIP-m cells did not affect sensitivity to 4-OH-tamoxifen, carboplatin, bortezomib, and X-ray radiation. These data suggest that SET plays important roles in the tumor progression of a subset of canine mammary tumor by suppressing PP2A activity and enhancing mTOR, β-catenin, and NFκB signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Canine mammary tumor cell lines CIP-p (primary origin) and CIP-m (metastatic origin), which previously generated from the same individual (Shih Tzu) 18 , were cultured in RPMI 1640 containing 10% FBS and 1x antibiotic/antimycotic (Life Technologies, Carlsbad, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

The role of SET/I2PP2A in canine mammary tumors

Kake

Tsuji

Enjoji

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Canine mammary tumor cell lines used in this study were established from primary tumors diagnosed as carcinoma (CMT1, CMT-U27, CMT9, P114, CHMp, CNMp and CIPp) or its metastasis (CHMm, CNMm and CIPm), benign mixed tumor (CMT-U229) and osteosarcoma-like tumor (CMT-U335) [19]–[21]. All cell lines were cultured in DMEM/F12 (Invitrogen, Bleiswijk, The Netherlands) supplemented with 10% fetal bovine serum (FBS) (FBS Gold, PAA, Cölbe, Germany).…”

Section: Methodsmentioning

confidence: 99%

Ligand-Independent Canonical Wnt Activity in Canine Mammary Tumor Cell Lines Associated with Aberrant LEF1 Expression

et al. 2014

View full text Add to dashboard Cite

Pet dogs very frequently develop spontaneous mammary tumors and have been suggested as a good model organism for breast cancer research. In order to obtain an insight into underlying signaling mechanisms during canine mammary tumorigenesis, in this study we assessed the incidence and the mechanism of canonical Wnt activation in a panel of 12 canine mammary tumor cell lines. We show that a subset of canine mammary cell lines exhibit a moderate canonical Wnt activity that is dependent on Wnt ligands, similar to what has been described in human breast cancer cell lines. In addition, three of the tested canine mammary cell lines have a high canonical Wnt activity that is not responsive to inhibitors of Wnt ligand secretion. Tumor cell lines with highly active canonical Wnt signaling often carry mutations in key members of the Wnt signaling cascade. These cell lines, however, carry no mutations in the coding regions of intracellular Wnt pathway components (APC, β-catenin, GSK3β, CK1α and Axin1) and have a functional β-catenin destruction complex. Interestingly, however, the cell lines with high canonical Wnt activity specifically overexpress LEF1 mRNA and the knock-down of LEF1 significantly inhibits TCF-reporter activity. In addition, LEF1 is overexpressed in a subset of canine mammary carcinomas, implicating LEF1 in ligand-independent activation of canonical Wnt signaling in canine mammary tumors. We conclude that canonical Wnt activation may be a frequent event in canine mammary tumors both through Wnt ligand-dependent and novel ligand–independent mechanisms.

show abstract

“…Canine mammary cell line CNMm was kindly provided by Prof. N. Sasaki [24]. This cell line is derived from a metastatic regional lymph node of a canine mammary carcinoma characterized by clinical stage II and a tubular morphology.…”

Section: Pr-b Expressing Cell Lines and Culturementioning

confidence: 99%