Abstract��OBJECTIVE To explore whether knockdown serglycin's expression level in MDA-MB-231 cells by transient transfection can improve the sensitivity of breast cancer cells to the doxorubicin.METHODS At first, qRT-PCR,Western-Blot and immunofluorescence were used to examine the expression level in two different cell lines, MDA-MB-231 and MCF-7. Then serglycin's expression level in MDA-MB-231 was knocked down by using transient transfection, qRT-PCR and immunofluorescence were used to test the efficiency of this approach; and then, between the NC group and the Si-SG group, MTS was used to measure the IC50 of doxorubicin and the proliferation curve under the treatment of the doxorubicin. Also the numbers of colony formation in this two groups was observed when treating with different concentration of doxorubicin. RESULTS It was found that in these two cells, the expression of serglycin in MDA-MB-231 is significantly higher than MCF-7. The efficiency of knockdown in MDA-MB-231 is above 70%. In Si-SG group, the IC50 and the growth curve under treatment with doxorubicin is significantly lower than the NC group. Same RESULTS can be found in the colony formation assay, when treating with the doxorubicin, the decreasing rate of colony numbers is significantly quicker in the Si-SG group than NC group. CONCLUSION Knockdown serglycin's expression level in MDA-MB-231 cells by transient transfection can improve the sensitivity to the doxorubicin.
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CAO Li, LIU Tao, CHEN Zhuo-jia, JIA Shou-wei, HUANG Bi-jun, HUANG Hong-bing. Investigation the Importance of Serglycinin the Drug-Resistance to the Doxorubicin in Breast Cancer. Chinese Pharmaceutical Journal, 2017, 52(4): 284-287.
SINGLETARY K W, GAPSTUR S M. Alcohol and breast cancer:review of epidemiologic and experimental evidence and potential mechanisms[J]. JAMA, 2001, 286(17):2143-2151.
[2]
KELSEY J L. A review of the epidemiology of human breast cancer[J]. Epidemiol Rev, 1979, 1(1):74-109.
[3]
National Comprehensive Cancer Network. Breast cancer clinical practice guidelines in oncology[J]. J Nat Compr Cancer Network, 2003, 1(2):148-188.
[4]
GOTTESMAN M M. Mechanisms of cancer drug resistance[J]. Ann Rev Med, 2002, 53(1):615-627.
[5]
KORPETINOU A, PAPACHRISTOU D J, LAMPROPOULOU A, et al. Increased expression of serglycin in specific carcinomas and aggressive cancer cell lines[J]. Biomed Res Int, 2015, 2015(10):1-10.
[6]
KOLSET S O, TVEIT H. Serglycin-structure and biology[J]. Cell Mol Life Sci, 2008, 65(7-8):1073-1085.
[7]
KORPETINOU A, SKANDALIS S S, MOUSTAKAS A, et al. Serglycin is implicated in the promotion of aggressive phenotype of breast cancer cells[J]. PLoS One, 2013, 8(10):e78157.
[8]
LI X J, QIAN C N. Serglycin in human cancers[J]. Chin J Cancer(��֢), 2011, 30(9):585-589.
[9]
NIEMANN C U, KJELDSEN L, RALFKIAER E, et al. Serglycin proteoglycan in hematologic malignancies:a marker of acute myeloid leukemia[J]. Leukemia, 2007, 21(12):2406-2410.
[10]
THEOCHARIS A D, SEIDEL C, BORSET M, et al. Serglycin constitutively secreted by myeloma plasma cells is a potent inhibitor of bone mineralization in vitro[J]. J Biol Chem, 2006, 281(46):35116-35128.
[11]
LI X J, ONG C K, CAO Y, et al. Serglycin is a theranostic target in nasopharyngeal carcinoma that promotes metastasis[J]. Cancer Res, 2011, 71(8):3162-3172.
[12]
CHIA C S, ONG W S, LI X J, et al. Serglycin expression:an independent marker of distant metastases in nasopharyngeal carcinoma[J]. Head Neck, 2016, 38(1):21-28.
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