IndraLab

Statements

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"XREF_BIBR Overexpression of TREK-1 in healthy prostate epithelial cells increased their proliferation ability."
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"XREF_BIBR In contrast, the knockdown of TREK-1 significantly inhibited the proliferation of prostate cancer cells."
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"Furthermore, TREK-1 inhibits proliferation of neuronal stem cells, astrocytes, osteoblasts, Chinese hamster ovary cells, and neonatal cardiomyocytes, but increases the proliferation of prostate cancer cell lines."
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"The two-pore domain K + channel, TREK1, increases proliferation of PC-3 and LNCaP prostate cancer cells."
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"TASK-3 or TREK-1 overexpression leads to proliferation on embryonic fibroblast (C8) and Chinese hamster ovary (CHO) cell lines, respectively."
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"In vitro, ablation of TREK-1 alters the cytokine release profile of alveolar epithelial cells upon TNF-α stimulation (e.g., ↓IL-6 and ↑MCP-1) and increases the proliferation of alveolar epithelial cells."
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"Furthermore, knockdown of TREK-1 significantly inhibited PCa cell proliferation in vitro and in vivo, and induced a G1/S cell cycle arrest."
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"Taken together, our results demonstrated that TREK-1 knockdown inhibited cell proliferation of PCa cells."
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"The authors also found that TREK-1 blockers could inhibit cell proliferation of ovarian cancer cells through reducing early apoptosis and increasing late apoptosis."
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"The fact that TREK-1 contributes to cell proliferation might in part explain our finding that TREK-1 expression was positively associated with GS and T staging."
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"Taken together, these findings propose a model where under conditions of pressure overload, TREK-1 mediates the activation of JNK and thereby limits excessive cardiomyocyte hypertrophy by reducing hyp[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Knockdown of TREK-1 significantly inhibited the proliferation of prostate cancer cells both in vitro and in vivo (Zhang et al., 2015)."
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"TASK channels are expressed in lymphocytes, where they could contribute to inflammatory responses [55], and TASK-3 and TREK-1 are overexpressed in breast and prostate cancer cells, where they support cell proliferation and tumorigenesis [56,57]."
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"In addition, BrdU incorporation assay revealed that the siRNA knockdown of TREK1 significantly reduced the proliferation of LX-2 cells at 72 h (0.922 ± 0.053, n = 4, p = 0.007 vs. control, 1.130 ± 0.0[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"TREK-1 overexpression has also been shown to promote ovarian and prostate cancer cell proliferation [44,45] ."
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"This hypothesis was substantiated by the knockdown of TREK1 channels inhibiting the proliferation of LX-2 cells ( Fig. 7 )."
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"The proliferation and migration of IPAH-PASMCs were inhibited by KCNK channel blockers and by the siRNA knockdown of KCNK1 or KCNK2 channels."
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"In both prostate [125] and ovarian cancer [220], the inhibition or knockdown of K 2.1 inhibits proliferation by inducing cell cycle arrest at the G /S checkpoint."
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"The excessive proliferation was inhibited by the siRNA knockdown of KCNK1 (20.5 ± 1.8% decrease, n = 28, p < 0.001 vs. control siRNA, n = 28) or KCNK2 (33.5 ± 2.0% decrease, n = 28, p < 0.001 vs. control siRNA, n = 28) for 48 h (Figures 7C,D)."
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"For instance, in ovarian cancer, certain regulators of KCNK2 have been shown to inhibit apoptosis and to promote cell proliferation (54)."
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"For instance, some KCNK2 modulators inhibit apoptosis and promote proliferation in ovarian cancer [14]."
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"TREK-1 overexpression increases the proliferation of normal prostate epithelial cells, which can be reduced by a TREK-1 inhibitor or expression of dominant-negative TREK-1 [ 87 ]."
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"142 In prostate cancer, inhibition or knockdown of TREK-1 inhibits proliferation by inducing cell cycle arrest at the G1/S checkpoint.142 On the other side, the treatment with TREK-1-blocking agents, such as curcumin, has shown reduced ovarian cancer cells proliferation and increased late apoptosis processes.130Among the TREK subfamily, the TREK-2 channel (K2P10, encoded by KCNK10) was present in bladder cancer cell lines and contributed to cell cycle-dependent growth."
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"In addition, TREK-1 knockdown significantly attenuated prostate cancer cell proliferation both in vitro and in vivo."
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