Reduction of breast cancer cell migration via up‐regulation of TASK‐3 two‐pore domain K<sup>+</sup> channel

Lee, G.-W.; Park, H. S.; Kim, Eun‐Jung; Cho, Y.-W.; Kim, G.-T.; Mun, Yun-Ja; Choi, Eunju; Lee, J.-S.; Han, Jae Hee; Kang, Dawon

doi:10.1111/j.1748-1716.2011.02359.x

Cited by 37 publications

(34 citation statements)

References 23 publications

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“…In the present study, LRRC3B expression levels decreased in breast cancer MDA-MB-231 and MCF-7 cells that were treated with different concentrations of bupivacaine, indicating that the administration of bupivacaine to breast cancer tumor cells suppressed the expression of LRRC3B. A number of studies have revealed that bupivacaine administration during cancer surgery serves a crucial role in cancer recurrence and metastasis by promoting cell migration (27,28). In line with previous studies, the data of the present study showed that 50 µg/ml bupivacaine yielded the maximum increase breast cell invasion.…”

Section: Discussionmentioning

confidence: 94%

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Kong

Zou

2017

Oncology Letters

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Abstract. The present study aimed to investigate the potential effect of leucine-rich repeat containing 3B (LRRC3B) with respect to the inhibition of breast cancer recurrence and metastasis post-anesthesia. The mRNA expression of LRRC3B in breast MDA-MB-231 and MCF-7 cell lines was detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. The effect of bupivacaine on breast cancer cell invasion was analyzed using a Matrigel assay. LRRC3B specific small interfering (si)RNA was constructed and transfected into breast cancer cells using Lipofectamine ® 2000 reagent. The influence of bupivacaine on LRRC3B expression was measured based on RT-qPCR. Additionally, the effect of LRRC3B silencing on the invasion of breast cancer cells treated with bupivacaine was analyzed. Compared with the control, LRRC3B expression significantly increased in MDA-MB-231 and in MCF-7 cells as the length of time increased (P<0.05), but the expression of the gene significantly declined in 2 types of cancer cell when the cells were transfected with siRNA-LRRC3B plasma (P<0.05). The administration of 50 µg/ml bupivacaine promoted maximum breast cancer cell invasion, and suppressed LRRC3B mRNA expression in cells. However, when LRRC3B was silenced in cancer cells, 20 µg/ml bupivacaine significantly promoted cancer cell invasion, indicating that bupivacaine suppresses the expression of LRRC3B and promotes cell invasion. The present study suggested that LRRC3B serves a protective role in preventing bupivacaine-induced breast cancer recurrence and metastasis.

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Section: Discussionmentioning

confidence: 94%

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Kong

Zou

2017

Oncology Letters

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“…Incidence of PDAC correlates with increasing age and therefore is an increasing problem as world population is aging [16]. Dysfunction of ion channels is an emerging field in cancer research and differential expression of multiple classes of ion channels has been reported for different cancer tissues [20–22, 28, 29, 31, 35, 43]. Plasma membrane ion channels are involved in apoptosis [19], differentiation, and proliferation [17, 28], and are further associated with cell migration [15, 38] and cell volume regulation [14].…”

Section: Introductionmentioning

confidence: 99%

ANO1 (TMEM16A) in pancreatic ductal adenocarcinoma (PDAC)

Sauter

Novak

Pedersen

et al. 2014

Pflugers Arch - Eur J Physiol

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Pancreatic ductal adenocarcinoma (PDAC) has one of the worst survival rates of all cancers. ANO1 (TMEM16A) is a recently identified Ca2+-activated Cl− channel (CaCC) that is upregulated in several tumors. Although ANO1 was subject to extensive studies in the recent years, its pathophysiological function has only been poorly understood. The aim of the present study is to establish the significance of ANO1 in PDAC behavior and demarcate its roles in PDAC from those of the volume-regulated anion channel (VRAC). We performed qPCR and Western blot measurements on different PDAC cell lines (Panc-1, Mia PaCa 2, Capan-1, AsPC-1, BxPC-3) and compared the results to those obtained in a human pancreatic ductal epithelium (HPDE) cell line. All cancer cell lines showed an upregulation of ANO1 on mRNA and protein levels. Whole-cell patch-clamp recordings identified large Ca2+ and voltage-dependent Cl− currents in PDAC cells. Using siRNA knockdown of ANO1 and three ANO1 inhibitors (T16Ainh-A01, CaCCinh-A01, and NS3728), we found that ANO1 is the main constituent of CaCC current in PDAC cells. We further characterized these three inhibitors and found that they had unspecific effects on the free intracellular calcium concentration. Functional studies on PDAC behavior showed that surprisingly inhibition of ANO1 did not influence cellular proliferation. On the other hand, we found ANO1 channel to be pivotal in PDAC cell migration as assessed in wound healing experiments.Electronic supplementary materialThe online version of this article (doi:10.1007/s00424-014-1598-8) contains supplementary material, which is available to authorized users.

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“…Within the K V family, K V 11.1 (hERG) shows altered expression in an array of cancer types and has been shown to impact cellular proliferation (melanoma, colorectal cancer and Barrett's esophagus), migration (melanoma, thyroid and breast cancer), malignant transformation (head & neck carcinoma) and apoptosis (gastric cancer). While K V 11.1 is most frequently reported for its role in cancer, an array of other K + channels have also been proposed as molecular components promoting cancer development and progression [9], [10], [24]–[80] (summarised in Table 1). …”

Section: Introductionmentioning

confidence: 99%

Altered Expression of Two-Pore Domain Potassium (K2P) Channels in Cancer

2013

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Potassium channels have become a focus in cancer biology as they play roles in cell behaviours associated with cancer progression, including proliferation, migration and apoptosis. Two-pore domain (K2P) potassium channels are background channels which enable the leak of potassium ions from cells. As these channels are open at rest they have a profound effect on cellular membrane potential and subsequently the electrical activity and behaviour of cells in which they are expressed. The K2P family of channels has 15 mammalian members and already 4 members of this family (K2P2.1, K2P3.1, K2P9.1, K2P5.1) have been implicated in cancer. Here we examine the expression of all 15 members of the K2P family of channels in a range of cancer types. This was achieved using the online cancer microarray database, Oncomine (www.oncomine.org). Each gene was examined across 20 cancer types, comparing mRNA expression in cancer to normal tissue. This analysis revealed all but 3 K2P family members (K2P4.1, K2P16.1, K2P18.1) show altered expression in cancer. Overexpression of K2P channels was observed in a range of cancers including breast, leukaemia and lung while more cancers (brain, colorectal, gastrointestinal, kidney, lung, melanoma, oesophageal) showed underexpression of one or more channels. K2P1.1, K2P3.1, K2P12.1, were overexpressed in a range of cancers. While K2P1.1, K2P3.1, K2P5.1, K2P6.1, K2P7.1 and K2P10.1 showed significant underexpression across the cancer types examined. This analysis supports the view that specific K2P channels may play a role in cancer biology. Their altered expression together with their ability to impact the function of other ion channels and their sensitivity to environmental stimuli (pO2, pH, glucose, stretch) makes understanding the role these channels play in cancer of key importance.

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Reduction of breast cancer cell migration via up‐regulation of TASK‐3 two‐pore domain K⁺ channel

Abstract: These results show that an increase in TASK-3 expression levels, which could be modulated by PKC activation, reduces cell migration/invasion in breast cancer cells and suggest that modulation of TASK-3 expression may regulate metastasis of breast cancer cells.

Cited by 37 publications

References 23 publications

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

ANO1 (TMEM16A) in pancreatic ductal adenocarcinoma (PDAC)

Altered Expression of Two-Pore Domain Potassium (K2P) Channels in Cancer

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Reduction of breast cancer cell migration via up‐regulation of TASK‐3 two‐pore domain K+ channel

Abstract: These results show that an increase in TASK-3 expression levels, which could be modulated by PKC activation, reduces cell migration/invasion in breast cancer cells and suggest that modulation of TASK-3 expression may regulate metastasis of breast cancer cells.

Cited by 37 publications

References 23 publications

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

Protective role of LRRC3B in preventing breast cancer metastasis and recurrence post-bupivacaine

ANO1 (TMEM16A) in pancreatic ductal adenocarcinoma (PDAC)

Altered Expression of Two-Pore Domain Potassium (K2P) Channels in Cancer

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Reduction of breast cancer cell migration via up‐regulation of TASK‐3 two‐pore domain K⁺ channel