Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer

Lu, Chengli; Ma, Zhiyuan; Cheng, Xiaoming; Wu, Huichao; Tuo, Biguang; Liu, Xuemei; Li, Taolang

doi:10.1186/s12935-020-01464-9

Cited by 13 publications

(10 citation statements)

References 122 publications

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“…AQP5 is involved in normal mammary development and milk production, as well as in breast carcinogenesis [80,98]. Jung et al showed that silencing of AQP5 or induction of hyperosmotic stress to MCF-7 cells decreases the expression of AQP5 and negatively affects cell proliferation and migration.…”

Section: Aqp5 and Breast Cancermentioning

confidence: 99%

AQP3 and AQP5—Potential Regulators of Redox Status in Breast Cancer

Milković

Gašparović

2021

Molecules

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Breast cancer is still one of the leading causes of mortality in the female population. Despite the campaigns for early detection, the improvement in procedures and treatment, drastic improvement in survival rate is omitted. Discovery of aquaporins, at first described as cellular plumbing system, opened new insights in processes which contribute to cancer cell motility and proliferation. As we discover new pathways activated by aquaporins, the more we realize the complexity of biological processes and the necessity to fully understand the pathways affected by specific aquaporin in order to gain the desired outcome–remission of the disease. Among the 13 human aquaporins, AQP3 and AQP5 were shown to be significantly upregulated in breast cancer indicating their role in the development of this malignancy. Therefore, these two aquaporins will be discussed for their involvement in breast cancer development, regulation of oxidative stress and redox signalling pathways leading to possibly targeting them for new therapies.

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Section: Aqp5 and Breast Cancermentioning

confidence: 99%

AQP3 and AQP5—Potential Regulators of Redox Status in Breast Cancer

Milković

Gašparović

2021

Molecules

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“…Recent studies have described that altered expression or activity of ion transporters play an important role in the development or progression of different types of cancer [22][23][24][25][26]. For this reason, many ion transporters emerged as potential targets for cancer therapy [27,28].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Becskeházi

Korsós

Gál

et al. 2021

IJMS

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Several clinical studies indicate that smoking predisposes its consumers to esophageal inflammatory and malignant diseases, but the cellular mechanism is not clear. Ion transporters protect esophageal epithelial cells by maintaining intracellular pH at normal levels. In this study, we hypothesized that smoking affects the function of ion transporters, thus playing a role in the development of smoking-induced esophageal diseases. Esophageal cell lines were treated with cigarettesmoke extract (CSE), and the viability and proliferation of the cells, as well as the activity, mRNA and protein expression of the Na+/H+ exchanger-1 (NHE-1), were studied. NHE-1 expression was also investigated in human samples. For chronic treatment, guinea pigs were exposed to tobacco smoke, and NHE-1 activity was measured. Silencing of NHE-1 was performed by using specific siRNA. CSE treatment increased the activity and protein expression of NHE-1 in the metaplastic cells and decreased the rate of proliferation in a NHE-1-dependent manner. In contrast, CSE increased the proliferation of dysplastic cells independently of NHE-1. In the normal cells, the expression and activity of NHE-1 decreased due to in vitro and in vivo smoke exposure. Smoking enhances the function of NHE-1 in Barrett’s esophagus, and this is presumably a compensatory mechanism against this toxic agent.

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“…SOCE inhibitors in early preclinical studies have demonstrated an ability to inhibit proliferation and migration in MDA-MB-231 TNBC cell lines and reduce tumour growth in TNBC mouse models [50] . In addition, Azimi et al (2017) observed that TRPC1 is significantly increased in TNBC compared to all other BC subtypes, resulting in an enhanced epithelial-mesenchymal transition (EMT) phenotype [51] . Going forward, this review focuses on the role of Ca 2+ in supporting TSGs and oncogenes commonly altered in TNBC; however, altered calcium channel expression in BC subtypes has been extensively reviewed elsewhere [24,46,52] .…”

Section: The Role Of Calcium In Cancermentioning

confidence: 99%

“…Induction of SNAIL expression is known to mediate EMT, a cellular phenotype linked to drug resistance [126,127] . In addition, TRPC1 has also been shown to play a role in EMT of TNBC via regulation of hypoxia-inducible factor 1 alpha (HIF-1α) and AKT signalling in PTEN-deficient BC cells [51] . Azimi et al also noted that TRPC1 has a prognostic value in basal BC a molecular subtype associated with TNBC [51] .…”

Section: The Role That Calcium Plays On the Impact Of Tp53 Mutations ...mentioning

confidence: 99%

Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer

Eustace¹,

Lee²,

Colley³

et al. 2022

Cancer Drug Resist

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Triple-negative breast cancer (TNBC) is characterized as an aggressive form of breast cancer (BC) associated with poor patient outcomes. For the majority of patients, there is a lack of approved targeted therapies. Therefore, chemotherapy remains a key treatment option for these patients, but significant issues around acquired resistance limit its efficacy. Thus, TNBC has an unmet need for new targeted personalized medicine approaches. Calcium (Ca2+) is a ubiquitous second messenger that is known to control a range of key cellular processes by mediating signalling transduction and gene transcription. Changes in Ca2+ through altered calcium channel expression or activity are known to promote tumorigenesis and treatment resistance in a range of cancers including BC. Emerging evidence shows that this is mediated by Ca2+, modulation supporting the function of tumour suppressor genes (TSGs) and oncogenes. This review provides insight into the underlying alterations in calcium signalling and how it plays a key role in promoting disease progression and therapy resistance in TNBC which harbours mutations in tumour protein p53 (TP53) and the PI3K/AKT pathway.

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Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer

Cited by 13 publications

References 122 publications

AQP3 and AQP5—Potential Regulators of Redox Status in Breast Cancer

AQP3 and AQP5—Potential Regulators of Redox Status in Breast Cancer

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer

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