Comparative changes in breast cancer cell proliferation and signalling following somatostatin and cannabidiol treatment

被引:5
作者
Oliveira, Helen A. [1 ]
Somvanshi, Rishi K. [1 ,2 ]
Kumar, Ujendra [1 ,2 ]
机构
[1] Univ British Columbia, Fac Pharmaceut Sci, Vancouver, BC, Canada
[2] Univ British Columbia, Fac Pharmaceut Sci, Vancouver, BC V6T 1Z3, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
MDA-MB-231; cells; MCF-7; Somatostatin; Cannabinoids; Proliferation and apoptosis; Signalling pathways; CANNABINOIDS; INHIBITION; GROWTH; EXPRESSION; APOPTOSIS; RECEPTORS; EMPHASIS;
D O I
10.1016/j.bbrc.2022.12.073
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Breast cancer is the most commonly diagnosed cancer and a leading cause of cancer-related death among women worldwide. Somatostatin (SST) and Cannabinoids have an anti-proliferative and pro-apoptotic effect, but the mechanisms of their actions remain elusive. In the present study, we have evaluated the effects of SST, Cannabidiol (CBD) alone or in combination on receptor expression, cell proliferation and apoptosis and related downstream signalling pathways in MDA-MB-231 and MCF-7 breast cancer cells. The results presented here demonstrate the cell type and agonist-dependent changes in receptor expression at the cell membrane, inhibition of cell proliferation and increased apoptosis following treatment with SST and CBD alone and in combination. In comparison to MDA-MB-231 cells, MCF-7 cells treated with SST alone and in combination with CBD exhibited inhibition of phosphorylated Protein Kinase B (pAKT) and phosphorylated-Phosphoinositide 3-Kinase (pPI3K) expression. Importantly, inhi-bition of PI3K/AKT activation was accompanied by enhanced PTEN expression in MCF-7 cells. These results highlight the possible interaction between SSTR and CBR subtypes with the implication in the modulation of receptor expression, cell viability and signal transduction pathways in a breast cancer cell type-dependent manner.(c) 2022 Elsevier Inc. All rights reserved.
引用
收藏
页码:30 / 38
页数:9
相关论文
共 41 条
  • [1] Regulatory Mechanisms of Somatostatin Expression
    Ampofo, Emmanuel
    Nalbach, Lisa
    Menger, Michael D.
    Laschke, Matthias W.
    [J]. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2020, 21 (11) : 1 - 15
  • [2] Δ9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation
    Caffarel, Maria M.
    Sarrio, David
    Palacios, Jose
    Guzman, Manuel
    Sanchez, Cristina
    [J]. CANCER RESEARCH, 2006, 66 (13) : 6615 - 6621
  • [3] Cannabinoids: A new hope for breast cancer therapy?
    Caffarel, Maria M.
    Andradas, Clara
    Perez-Gomez, Eduardo
    Guzman, Manuel
    Sanchez, Cristina
    [J]. CANCER TREATMENT REVIEWS, 2012, 38 (07) : 911 - 918
  • [4] Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition
    Caffarel, Maria M.
    Andradas, Clara
    Mira, Emilia
    Perez-Gomez, Eduardo
    Cerutti, Camilla
    Moreno-Bueno, Gema
    Flores, Juana M.
    Garcia-Real, Isabel
    Palacios, Jose
    Manes, Santos
    Guzman, Manuel
    Sanchez, Cristina
    [J]. MOLECULAR CANCER, 2010, 9
  • [5] Cannabinoids as therapeutic agents in cancer: current status and future implications
    Chakravarti, Bandana
    Ravi, Janani
    Ganju, Ramesh K.
    [J]. ONCOTARGET, 2014, 5 (15) : 5852 - 5872
  • [6] PTEN: Tumor Suppressor and Metabolic Regulator
    Chen, Chien-Yu
    Chen, Jingyu
    He, Lina
    Stiles, Bangyan L.
    [J]. FRONTIERS IN ENDOCRINOLOGY, 2018, 9
  • [7] Function of Akt/PKB signaling to cell motility, invasion and the tumor stroma in cancer
    Chin, Y. Rebecca
    Toker, Alex
    [J]. CELLULAR SIGNALLING, 2009, 21 (04) : 470 - 476
  • [8] Reduced PTEN expression in breast cancer cells confers susceptibility to inhibitors of the PI3 kinase/Akt pathway
    deGraffenried, LA
    Fulcher, L
    Friedrichs, WE
    Grünwald, V
    Ray, RB
    Hidalgo, M
    [J]. ANNALS OF ONCOLOGY, 2004, 15 (10) : 1510 - 1516
  • [9] Prevention of hormone-related cancers: Breast cancer
    Dunn, BK
    Wickerham, L
    Ford, LG
    [J]. JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (02) : 357 - 367
  • [10] Feng Y., Genes diseases