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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Exp+Clin+Cancer+Res
2019 ; 38
(1
): 106
Nephropedia Template TP
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TRPM7 promotes the epithelial-mesenchymal transition in ovarian cancer through
the calcium-related PI3K / AKT oncogenic signaling
#MMPMID30819230
Liu L
; Wu N
; Wang Y
; Zhang X
; Xia B
; Tang J
; Cai J
; Zhao Z
; Liao Q
; Wang J
J Exp Clin Cancer Res
2019[Feb]; 38
(1
): 106
PMID30819230
show ga
BACKGROUND: The epithelial-mesenchymal transition (EMT) is crucial for metastasis
and positively regulated by calcium-related signaling. The melastatin-related
transient receptor potential 7 (TRPM7) regulates a non-selective cation channel
and promotes cancer metastasis. However, the mechanisms underlying the action of
TRPM7 in ovarian cancer are unclear. METHODS: The expression of TRPM7 and EMT
markers (Vimentin, N-cadherin, Twist and E-cadherin) in ovarian cancer samples
was detected. TRPM7was knockdown by shRNA in Ovarian cancer cell lines to examine
calcium [Ca2+]i, EMT markers and PI3K/AKT markers. Various cellular assays, such
as invasion and migration, were performed in vitro, and further confirmed in
vivo. RESULTS: TRPM7 expression is negatively correlated with E-cadherin, but
positively with N-cadherin, Vimentin and Twist expression in ovarian cancer
samples. TRPM7 depletion inhibited the migration and invasion in SKOV3 and OVCAR3
cells. In addition, TRPM7 silencing decreased the lung metastasis of SKOV3 tumors
and prolonged the survival of tumor-bearing mice. Similar to that of TRPM7
silencing, treatment with MK886, a potent 5-lipoxygenase inhibitor to reduce
TRPM7 expression, and/or BAPTA-AM, an intracellular calcium chelator,
significantly mitigated the Epidermal growth factor (EGF) or Insulin-like growth
factors (IGF)-stimulated migration, invasion, and the EMT in ovarian cancer cells
by decreasing the levels of intracellular calcium [Ca2+]i. Furthermore, treatment
with LY2904002, a PI3K inhibitor, also inhibited the migration, invasion, and
treatment with both LY2904002 and BAPTA-AM further enhanced their inhibition in
ovarian cancer cells. Moreover, treatment with BAPTA-AM mitigated the
IGF-stimulated migration, invasion, particularly in TRPM7-silenced ovarian cancer
cells. Finally, TRPM7 silencing attenuated the PI3K/AKT activation, which was
enhanced by BAPTA-AM, MK886 or LY2904002 treatment in ovarian cancer cells.
CONCLUSIONS: TRPM7 silencing inhibited the EMT and metastasis of ovarian cancer
by attenuating the calcium-related PI3k/AKT activation. Our findings suggest that
TRPM7 may be a therapeutic target for intervention of ovarian cancer.