Hormone‐Responsive Creatine Kinase in Normal and Neoplastic Mammary Glands<sup>a</sup>

Kaye, Alvin M.; Hallowes, R. C.; Cox, S A; Sluyser, M.

doi:10.1111/j.1749-6632.1986.tb16006.x

Cited by 21 publications

(16 citation statements)

References 25 publications

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“…High CK-BB levels in breast tissue tend to occur in steroid hormone receptorpositive cancer (Scambia et al, 1986b(Scambia et al, , 1988 but not all published results agree (Kaye et al, 1986). We recently reported that CK-BB is associated with the ER (Zarghami et al, 1995).…”

Section: Discussionsupporting

confidence: 59%

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Zarghami

Giai²,

Yu³

et al. 1996

Br J Cancer

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Section: Discussionsupporting

confidence: 59%

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Zarghami

Giai²,

Yu³

et al. 1996

Br J Cancer

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“…Estrogen injection into immature rats causes a doubling of the weight of their uteri in 24 hr and, within 1 hr after estrogen injection, the concentration of mRNA for uterine CK-BB begins to increase (1). Other hormones and growth factors stimulate CK-BB activity in their target cells (2). Increased CK activity has been observed in regenerating rat liver (3), and CK has been implicated in spindle activity during normal cell division (4).…”

mentioning

confidence: 99%

Inhibition of rate of tumor growth by creatine and cyclocreatine.

Miller

Evans

Cohn

1993

Proc. Natl. Acad. Sci. U.S.A.

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Growth rate inhibition of subcutaneously implanted tumors results from feeding rats and athymic nude mice diets containing 1% cyclocreatine or 1%, 2%, 5%, or 10% creatine. The tumors studied included rat mammary tumors (Ac33tc in Lewis female rats and 13762A in Fischer 344 female rats), rat sarcoma MCI in Lewis male rats, and tumors resulting from the i jection of two human neuroblastoma cell lines, IMR-5 and CHP-134, in athymic nude mice. Inhibition was observed regardless of the time experimental diets were administered, either at the time of tumor implantation or after the appearance of palpable tumors. For mammary tumor Ac33tc, the growth inhibition during 24 days after the implantation was -50% for both 1% cyclocreatine and 1% creatine, and inhibition increased as creatine was increased from 2% to 10% of the diet. For the other rat mammary tumor (13762A), there was -35% inhibition by both 1% cyclocreatine and 2% creatine. In the case of the MCI sarcoma, the inhibitory effect appeared more pronounced at earlier periods of growth, ranging from 26% to 41% for 1% cyclocreatine and from 30% to 53% for 1% creatine; there was no significant difference in growth rate between the tumors in the rats fed 1% and 5% creatine. The growth rate of tumors in athymic nude mice, produced by implantation of the human neuroblastoma IMR-5 cell line, appeared somewhat more effectively inhibited by 1% cyclocreatine than by 1% creatine, and 5% creatine feeding was most effective. For the CHP-134 cell line, 33% inhibition was observed for the 1% cyclocreatine diet and 71% for the 5% creatine diet. In several experiments, a delay in appearance of tumors was observed in animals on the experimental diets. In occasional experiments, neither additive inhibited tumor growth rate for the rat tumors or the athymic mouse tumors.

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“…genes, a (kb-processed pseudogene and a potential mitochondrial gene (4). CKM expression is usually restricted to differentiated skeletal and cardiac muscle (71), although it has also been reported to be expressed in the lens of the eye (M. B. Perryman, personal communication) and in certain carcinoma cells (35). CKB is expressed in a much broader range of tissues but at highest levels in brain.…”

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confidence: 99%

The upstream muscle-specific enhancer of the rat muscle creatine kinase gene is composed of multiple elements.

Horlick¹,

Benfield²

1989

Mol. Cell. Biol.

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A series of constructs that links the rat muscle creatine kinase promoter to the bacterial chloramphenicol acetyltransferase gene was generated. These constructs were introduced into differentiating mouse C2C12 myogenic cells to localize sequences that are important for up-regulation of the creatine kinase gene during myogenic differentiation. A muscle-specific enhancer element responsible for induction of chloramphenicol acetyltransferase expression during myogenesis was localized to a 159-base-pair region from 1,031 to 1,190 base pairs upstream of the transcription start site. Analysis of transient expression experiments using promoters mutated by deletion indicated the presence of multiple functional domains within this muscle-specific regulatory element. A DNA fragment spanning this region was used in DNase I protection experiments. Nuclear extracts derived from C2 myotubes protected three regions (designated El, E2, and E3) on this fragment from digestion, which indicated there may be three or more trans-acting factors that interact with the creatine kinase muscle enhancer. Gel retardation assays revealed that factors able to bind specifically to El, E2, and E3 are present in a wide variety of tissues and cell types. Transient expression assays demonstrated that elements in regions El and E3, but not necessarily E2, are required for full enhancer activity.

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Hormone‐Responsive Creatine Kinase in Normal and Neoplastic Mammary Glands^a

Cited by 21 publications

References 25 publications

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Inhibition of rate of tumor growth by creatine and cyclocreatine.

The upstream muscle-specific enhancer of the rat muscle creatine kinase gene is composed of multiple elements.

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Hormone‐Responsive Creatine Kinase in Normal and Neoplastic Mammary Glandsa

Cited by 21 publications

References 25 publications

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Creatine kinase BB isoenzyme levels in tumour cytosols and survival of breast cancer patients

Inhibition of rate of tumor growth by creatine and cyclocreatine.

The upstream muscle-specific enhancer of the rat muscle creatine kinase gene is composed of multiple elements.

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Hormone‐Responsive Creatine Kinase in Normal and Neoplastic Mammary Glands^a