ABSTRACT
Objective:To investigate the relationship between T/N take-up value and the clinic feature of breast cancer, and explore the predictive ability of T/N take-up value for breast cancer prognosis.Methods:Breast cancer patients treated at Zhongshan Hospital, Fudan University and undergoing BSGI examination before surgery from Jan 2014 to Nov 2018 were collected. The relationship between T/N take-up value and the clinical features of breast cancer and DFS was analyzed.Results:A total of 419 breast cancer patients were collected. The median follow-up time after operation was 34 months. At the end of the follow-up, 43 cases relapsed and 376 cases did not. The average T/N values of CC position and MLO position before surgery were 2.74 and 2.58. The T/N value of CC is related to tumor stage (χ 2=22.077, P<0.05), lymph node metastasis ( Z=2.138, P<0.05) and degree of invasion ( Z=3.371, P<0.05). The T/N value of MLO is related to tumor stage (χ 2=23.091, P<0.05), lymph node metastasis ( Z=2.531, P<0.05) and degree of invasion ( Z=2.99, P<0.05). The best cut-off values of CC position and MLO position calculated by ROC curve are 2.59 and 2.97. Univariate analysis showed that tumor staging ( HR: 2.039, 95% CI: 1.404-2.962, P=0.001), T/N value at CC position ( HR: 4.349, 95% CI: 2.141-8.883, P<0.001) and T/N value at MLO position ( HR: 2.767, 95% CI: 1.520-5.039, P<0.001) is an independent risk factor for the prognosis of breast cancer. Multivariate COX regression analysis showed that tumor stage ( HR: 1.959, 95% CI: 1.302-2.946, P=0.001) and T/N value at MLO position ( HR: 3.498, 95% CI: 1.531-7.992, P=0.003) are independent risk factor of breast cancer prognosis. Conclusion:The BSGI T/N value has a certain correlation with breast cancer DFS.
ABSTRACT
Objective:To investigate the effect of long non-coding RNA (LncRNA) LINC00672 on sensitivity of breast cancer to tamoxifen and related mechanisms.Methods:Human breast cancer MCF-7 cells was treated in vitro to establish tamoxifen resistance (resistance group) and corresponding parental cell line (parent group) . The interfered LINC00672 and control cell line were constructed by Crisper-cas9 in resistant cells. (Interference 1 group, interference 2 group and control group) . The expression of LINC00672, Akt and HER2 mRNA was determined by real-time quantitative PCR. The expression levels of total Akt (Akt-pan) , phosphorylation of Akt (p-Akt) and HER2 were detected by Western blot.CCK-8 assay was used to detect cell resistance to tamoxifen.Results:The expressions of LINC00672, Akt and HER2 mRNA in the parental group were (1.000±0.086) , (1.000±0.254) and (1.000±0.208) , and the TAM IC 50 was (1.417±0.153) μmol/L. The expressions of LINC00672, Akt and HER2 mRNA in the resistance group were (4.286±0.593) , (4.175±0.274) and (2.519±0.389) , and the TAM IC 50 was (12.029±1.016) μmol/L. The expressions of LINC00672, Akt and HER2 mRNA in the control group were (1.000±0.093) , (1.000±0.090) and (1.000±0.097) , and the TAM IC 50 was (10.58±0.639) μmol/L. The expressions of LINC00672, Akt and HER2 mRNA in the interference group 1 were (0.331±0.023) , (0.892±0.044) and (0.458±0.077) , and the TAM IC 50 was (6.250±0.836) μmol/L. The expressions of LINC00672, Akt and HER2 mRNA in the interference group 2 were (0.304±0.016) , (0.919±0.050) and (0.416±0.080) , and the TAM IC 50 was (4.764±0.553) μmol/L. As compared with the parental group, the expressions of LINC00672, Akt and HER2 mRNA were significantly up-regulated ( P<0.01) in resistance group, the protein levels of Akt-pan, p-Akt and HER2 was up-regulated. The IC 50 value of tamoxifen was significantly increased in resistance group ( P<0.01) . As compared with the control group, the expression levels of LINC00672 and HER2 mRNA were significantly decreased in the interference group 1 and the interference group 2 ( P<0.01) , the levels of Akt was not significantly changed ( P>0.05) . The protein levels of p-Akt and HER2 were significantly decreased but there was no significant change in the expression of Akt-pan. The IC50 value of tamoxifen was significantly decreased ( P<0.01) . Conclusion:LINC00672 may be involved in the formation of tamoxifen resistance in breast cancer cells, and its underlying mechanism is related to the promotion of HER2/p-Akt pathway.