scholarly journals Substance P/NK1R antagonistic effect of 17-Trifluoromethyl phenyl trinor prostaglandin F2α in Breast cancer

Author(s):  
Mayuri Mutukuru ◽  
Vijayakumar T.M

Abstract 17-Trifluoromethyl phenyl trinor prostaglandin F2α (17-TPGF2α) is extracted from Zinc data base, but its value for inhibiting breast cancer through SP/NK1R system remains unknown. This study was designed to investigate the potential antagonist effect of 17-TPGF2α through NK1Receptor. The effect of 17-TPGF2α on the proliferation and apoptosis of breast cancer cell lines were determined through invitro cell lines. Based on invitro results we planned to investigate anticancer activity in Female Balb/c and used SC injection of DMBA for cancer induction. Oral administration of 17-TPGF2α significantly suppress the tumor volume as compared with an untreated group. The serum parameters like ALP, AST and ALT and haematological parameters were normalized in test treated group. Histological examination revealed normal histoarchitecture of mammary gland and focal areas showed minimal inflammatory cell infiltration. There is no necrosis is seen both test treated and standard treated group when compared with Disease group. All these findings concluded that 17-TPGF2α may have potential as a novel antitumor candidate for breast cancer.

Alotrop ◽  
2017 ◽  
Vol 1 (1) ◽  
Author(s):  
Hermansyah Amir ◽  
Bambang Gonggo Murcitro

This study aimed to investigate research about cytotoxicity correlation level of Phaleria macrocarpa (Scheff) Boerl also known as Mahkota dewa leaves methanol extract against  MCF-7 cell in vitroto investigate the relationship between them in the goal to investigate alternative low cost herbal medicine agents to fight breast cancer. Cytotoxicity properties of samples against MCF-7 breast cancer cell lines was performed by using the Microtetrazolium (MTT) assay against MCF-7 cell line. The correlation between concentration of crude and cytotoxic activity was interpreted by statistical analyses. The study showed that P. macrocarpa leaves extracts showed cytoxicity activity against breast cancer MCF-7 cell lines which IC50 concentration showed at 15 µg/mL  Correlation between concentration of extract and cytotoxicity property (absorbance value) were founded in weak relationship (R = 0.372, R2 = 0.138).  It could be effect of many different compounds in the P. macrocarpa  leaves methanol extracts may cause the pharmacological interactions, so lower or higher concentration will be antagonistic effect on absorbance or cell viability. Further study on its mechanism pathway on revealing against breast cancer could be explored. Furthermore, the natural product derived from P. macrocarpa leaves methanol extracts have potential use as alternative drugs against breast cancer.


2019 ◽  
Vol 7 (19) ◽  
pp. 3169-3176
Author(s):  
Hussain Al Ssadh ◽  
Waleed Al Abdulmonem ◽  
Zafar Rasheed ◽  
Inamul Hasan Madar ◽  
Jamila Alhoderi ◽  
...  

BACKGROUND: The cluster of differentiation (CD) 74 is known for its immunological functions and its elevated level was reported in various cancer cells. AIM: The aim of the present study was to investigate the expression and potential roles of CD74 in the proliferative and apoptotic activity of breast cancer. METHODS: Expression of CD74, macrophage migration inhibitory factor (MIF) and CD44 was assayed in CAMA-1 and MDA-MB-231 cell lines using flow cytometry. CD74 was knocked down using CD74 siRNA-transfection in CAMA-1, and MDA-MB-231 cells and proliferation and apoptosis were determined in the transfected breast cancer cells. RESULTS: The data showed that CD74, MIF and CD44 were expressed in breast cancer cell lines and were associated with cell proliferation and apoptosis. Correlation analysis revealed that CD74 was positively correlated and colocalised with MIF on the cell-surface of CAMA-1 and MDA-MB-231. The knockdown of CD74 significantly reduced CAMA-1 and MDA-MB-231 cell proliferation and increased the level of apoptotic cells. CONCLUSION: We concluded that the interactions of CD74 with MIF and CD74 with CD44 could be a potential tumour marker for breast cancer cells. Moreover, the level of co-expression of MIF and CD74 or CD44 could be a surrogate marker for the efficacy of anti-angiogenic drugs, particularly in breast cancer tumours. In short, the study revealed the potential roles of CD74 in the proliferation and apoptosis of breast cancer which may serve as a potential therapeutic target for breast cancer.


2016 ◽  
Vol 36 (12) ◽  
pp. 6399-6408 ◽  
Author(s):  
LAMIA HAMDAN RAMDANI ◽  
OUALID TALHI ◽  
NADIA TAIBI ◽  
LAETITIA DELORT ◽  
CAROLINE DECOMBAT ◽  
...  

2021 ◽  
Author(s):  
In Hye Song ◽  
Young-Ae Kim ◽  
Sun-Hee Heo ◽  
Won Seon Bang ◽  
Hye Seon Park ◽  
...  

Abstract Background: The expression of major histocompatibility complex class I (MHC I) has previously been reported to be negatively associated with estrogen receptor (ER) expression. Furthermore, the expression of MHC I, the level of tumor-infiltrating lymphocytes (TILs), and the expression of interferon (IFN) mediator MxA are positively associated with one another in human breast cancers. This study aimed to investigate the mechanisms of association of MHC I with estrogen and IFN signaling. Methods: The human leukocyte antigen (HLA)-ABC protein expression was analyzed in breast cancer cell lines. The expressions of HLA-A and MxA mRNAs were analyzed in MCF-7 cells in Gene Expression Omnibus (GEO) data. ER and HLA-ABC expressions and TIL levels in tumor tissue were also analyzed in ER+/ human epidermal growth factor receptor 2 (HER2)- breast cancer patients who randomly received either neoadjuvant chemotherapy or estrogen modulator treatment following surgical resection. Results: HLA-ABC protein expression was decreased after β-estradiol treatment or hESR-GFP transfection and increased after fulvestrant or IFN-γ treatment in breast cancer cell lines. In GEO data, HLA-A and MxA expression was increased after ESR1 shRNA transfection. When comparing the two patient groups, ER Allred score was significantly lower and the HLA-ABC expression and TIL levels were significantly higher in the estrogen modulator treated group than the chemotherapy treated group. Conclusion: MHC I expression and TIL levels might be affected by ER pathway modulation and IFN treatment. Further studies elucidating the mechanism of MHC I regulation could suggest a way to boost TIL influx in cancer in a clinical setting.


2021 ◽  
Author(s):  
In Hye Song ◽  
Young-Ae Kim ◽  
Sun-Hee Heo ◽  
Won Seon Bang ◽  
Hye Seon Park ◽  
...  

Abstract Purpose: The expression of major histocompatibility complex class I (MHC I) has previously been reported to be negatively associated with estrogen receptor (ER) expression. Furthermore, the expression of MHC I, level of tumor-infiltrating lymphocytes (TILs), and expression of interferon (IFN) mediator MxA are positively associated with one another in human breast cancers. This study aimed to investigate the mechanisms of association of MHC I with estrogen and IFN signaling. Methods: The human leukocyte antigen (HLA)-ABC protein expression was analyzed in breast cancer cell lines. The expressions of HLA-A and MxA mRNAs were analyzed in MCF-7 cells in Gene Expression Omnibus (GEO) data. ER and HLA-ABC expressions and TIL levels in tumor tissue were also analyzed in ER+/ human epidermal growth factor receptor 2 (HER2)- breast cancer patients who randomly received either neoadjuvant chemotherapy or estrogen modulator treatment following surgical resection. Results: HLA-ABC protein expression was decreased after β-estradiol treatment or hESR-GFP transfection and increased after fulvestrant or IFN-γ treatment in breast cancer cell lines. In GEO data, HLA-A and MxA expression was increased after ESR1 shRNA transfection. When comparing the two patient groups, ER Allred score was significantly lower and the HLA-ABC expression and TIL levels were significantly higher in the estrogen modulator treated group than the chemotherapy treated group. Conclusion: MHC I expression and TIL levels might be affected by ER pathway modulation and IFN treatment. Further studies elucidating the mechanism of MHC I regulation could suggest a way to boost TIL influx in cancer in a clinical setting.


Sign in / Sign up

Export Citation Format

Share Document