TRP Channels: The Neglected Culprits in Breast Cancer Chemotherapy Resistance?

被引:1
作者
Soussi, Mayar [1 ]
Hasselsweiller, Alice [1 ]
Gkika, Dimitra [1 ]
机构
[1] Univ Lille, CHU Lille, Canc Heterogene Plast & Resistance Therapies, CNRS,Inserm,UMR9020,U1277,CANTHER, F-59000 Lille, France
关键词
breast cancer; TRP channels; chemotherapy; chemoresistance taxanes; anthracyclines; tamoxifen; DRUG-RESISTANCE; TAMOXIFEN RESISTANCE; DNA-DAMAGE; RECEPTOR; DOXORUBICIN; MECHANISMS; CELLS; INHIBITION; APOPTOSIS; ANTHRACYCLINES;
D O I
10.3390/membranes13090788
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 a major health concern worldwide, and resistance to therapies remains a significant challenge in treating this disease. In breast cancer, Transient Receptor Potential (TRP) channels are well studied and constitute key players in nearly all carcinogenesis hallmarks. Recently, they have also emerged as important actors in resistance to therapy by modulating the response to various pharmaceutical agents. Targeting TRP channels may represent a promising approach to overcome resistance to therapies in breast cancer patients.
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页数:13
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共 67 条
  • [1] Mechanisms of chemoresistance in cancer stem cells
    Abdullah, Lissa Nurrul
    Chow, Edward Kai-Hua
    [J]. CLINICAL AND TRANSLATIONAL MEDICINE, 2013, 2
  • [2] Molecular mechanisms and mode of tamoxifen resistance in breast cancer
    Ali, Shazia
    Rasool, Mahmood
    Chaoudhry, Hani
    Pushparaj, Peter N.
    Jha, Prakash
    Hafiz, Abdul
    Mahfooz, Maryam
    Sami, Ghufrana Abdus
    Kamal, Mohammad Azhar
    Bashir, Sania
    Ali, Ashraf
    Jamal, Mohammad Sarwar
    [J]. BIOINFORMATION, 2016, 12 (03) : 135 - 139
  • [3] Transient receptor potential A1 is a sensory receptor for multiple products of oxidative stress
    Andersson, David A.
    Gentry, Clive
    Moss, Sian
    Bevan, Stuart
    [J]. JOURNAL OF NEUROSCIENCE, 2008, 28 (10) : 2485 - 2494
  • [4] BCR-ABL-MEDIATED INHIBITION OF APOPTOSIS WITH DELAY OF G2/M TRANSITION AFTER DNA-DAMAGE - A MECHANISM OF RESISTANCE TO MULTIPLE ANTICANCER AGENTS
    BEDI, A
    BARBER, JP
    BEDI, GC
    ELDEIRY, WS
    SIDRANSKY, D
    VALA, MS
    AKHTAR, AJ
    HILTON, J
    JONES, RJ
    [J]. BLOOD, 1995, 86 (03) : 1148 - 1158
  • [5] Molecular mechanisms of anthracycline activity
    Beretta, Giovanni Luca
    Zunino, Franco
    [J]. ANTHRACYCLINE CHEMISTRY AND BIOLOGY II: MODE OF ACTION, CLINICAL ASPECTS AND NEW DRUGS, 2008, 283 : 1 - 19
  • [6] CAPSAZEPINE - A COMPETITIVE ANTAGONIST OF THE SENSORY NEURON EXCITANT CAPSAICIN
    BEVAN, S
    HOTHI, S
    HUGHES, G
    JAMES, IF
    RANG, HP
    SHAH, K
    WALPOLE, CSJ
    YEATS, JC
    [J]. BRITISH JOURNAL OF PHARMACOLOGY, 1992, 107 (02) : 544 - 552
  • [7] Poly(ADP-ribose)glycohydrolase is an upstream regulator of Ca2+ fluxes in oxidative cell death
    Blenn, C.
    Wyrsch, P.
    Bader, J.
    Bollhalder, M.
    Althaus, Felix R.
    [J]. CELLULAR AND MOLECULAR LIFE SCIENCES, 2011, 68 (08) : 1455 - 1466
  • [8] Burger H, 2003, CLIN CANCER RES, V9, P827
  • [9] Structural mechanisms of transient receptor potential ion channels
    Cao, Erhu
    [J]. JOURNAL OF GENERAL PHYSIOLOGY, 2020, 152 (03)
  • [10] Targeting autophagy to overcome drug resistance: further developments
    Chang, Haocai
    Zou, Zhengzhi
    [J]. JOURNAL OF HEMATOLOGY & ONCOLOGY, 2020, 13 (01)