Recombinant Human Granulocyte Colony-Stimulating Factor Promotes Preinvasive and Invasive Estrogen Receptor-Positive Tumor Development in MMTV-erbB2 Mice.
Recombinant Human Granulocyte Colony-Stimulating Factor Promotes Preinvasive and Invasive Estrogen Receptor-Positive Tumor Development in MMTV-erbB2 Mice.
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DOI：
10.4048/jbc.2015.18.2.126
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发表时间：
2015-06
影响因子：
2.4
通讯作者：
Feng XS
中科院分区：
文献类型：
--
作者：
Zhao CL;Zhang GP;Xiao ZZ;Ma ZK;Lei CP;Song SY;Feng YY;Zhao YC;Feng XS
我们研究了重组人粒细胞集落刺激因子（rhG-CSF）是否可以促进雌激素受体阳性肿瘤小鼠乳腺肿瘤病毒（MMTV-erbB 2）的侵袭前和侵袭性乳腺癌的发展。将MMTV-erbB 2小鼠随机分为3个实验组，每组20只。MMTV-erbB 2小鼠在3月龄时每日皮下注射溶媒或rhG-CSF（低rhG-CSF组，rhG-CSF 0.125 µg;溶媒-rhG-CSF组，生理盐水0.25 µg;高rhG-CSF组，rhG-CSF 0.25 µg）。通过免疫组化和逆转录聚合酶链反应研究了G-CSF在乳腺中作用的细胞和分子机制。低剂量rhG-CSF显著加速MMTV-erbB 2小鼠乳腺肿瘤的发生。rhG-CSF短期治疗可明显促进乳腺癌浸润前病变的发展。癌症预防效果与乳腺中增殖细胞核抗原、分化簇34和信号转导和转录激活因子3的表达降低> 80%相关。我们发现，在体外和体内，G-CSF都受到rhG-CSF的调节。G-CSF基因的鉴定有助于我们进一步了解G-CSF促进癌症的机制。低剂量rhG-CSF可显著延长肿瘤潜伏期，增加肿瘤多样性和肿瘤负荷。此外，rhG-CSF有效地促进MMTV-erbB 2小鼠的恶性和癌前乳腺病变的发展。
We investigated whether recombinant human granulocyte colony-stimulating factor (rhG-CSF) could promote the development of preinvasive and invasive breast cancer in mouse mammary tumor virus (MMTV-erbB2) mice with estrogen receptor-positive tumors. MMTV-erbB2 mice were randomly divided into three experimental groups with 20 mice in each group. MMTV-erbB2 mice were treated with daily subcutaneous injections of vehicle or rhG-CSF (low-rhG-CSF group, rhG-CSF 0.125 µg; vehicle-rhG-CSF group, normal saline 0.25 µg; and high-rhG-CSF group, rhG-CSF 0.25 µg) at 3 months of age. Cellular and molecular mechanisms of G-CSF action in mammary glands were investigated via immunohistochemistry and reverse transcription polymerase chain reaction. Low, but not high, rhG-CSF doses significantly accelerated mammary tumorigenesis in MMTV-erbB2 mice. Short-term treatment with rhG-CSF could significantly promote the development of preinvasive mammary lesions. The cancer prevention effect was associated with reduced expression of proliferating cell nuclear antigen, cluster of differentiation 34, and signal transducers and activators of transcription 3 in mammary glands by >80%. We found that G-CSF was regulated by rhG-CSF both in vitro and in vivo. Identification of G-CSF genes helped us further understand the mechanism by which G-CSF promotes cancer. Low doses of rhG-CSF could significantly increase tumor latency and increase tumor multiplicity and burden. Moreover, rhG-CSF effectively promotes development of both malignant and premalignant mammary lesions in MMTV-erbB2 mice.
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影响因子：
254.7
作者：
Jemal, Ahmedin;Siegel, Rebecca;Thun, Michael J.
通讯作者：
Thun, Michael J.
影响因子：
8.8
作者：
Kumar, J.;Fraser, F. W.;Riley, C.;Ahmed, N.;McCulloch, D. R.;Ward, A. C.
通讯作者：
Ward, A. C.
影响因子：
20.3
作者：
Hirbe, Angela C.;Uluckan, Ozge;Weilbaecher, Katherine
通讯作者：
Weilbaecher, Katherine
影响因子：
20.3
作者：
BASHEY, A;HEALY, L;MARSHALL, CJ
通讯作者：
MARSHALL, CJ
影响因子：
9.7
作者：
Savarese, TM;Mitchell, K;Quesenberry, PJ
通讯作者：
Quesenberry, PJ