Dehydrocrenatidine inhibits head and neck cancer cells invasion and migration by modulating JNK1/2 and ERK1/2 pathway and decreases MMP‐2 expression

Abstract

Head and neck cancer is associated with poor prognosis because of its highly metastatic nature. For the better management of head and neck cancer patients, it is very important to diagnose the cancer at an early stage, as well as to prevent the rapid spread of cancer either through direct invasion or lymphatic metastasis. In present study, the effect of dehydrocrenatidine, which is a beta‐carboline alkaloid found in the medicinal plant Picrasma quassioides, on human head and neck cancer metastasis was investigated. The study results revealed the treatment of FaDu, SCC9, and SCC47 cells with 5, 10, and 20 μM of dehydrocrenatidine significantly decreased the motility, migration, and invasion of head and neck cancer cells. Moreover, the dehydrocrenatidine treatment significantly decreased the expression of MMP‐2 and phosphorylation of ERK1/2 and JNK1/2. Additional experiments revealed that the cotreatment of dehydrocrenatidine with either ERK1/2 or JNK1/2 inhibitor caused further reduction in cancer cell motility and migration compared to that in dehydrocrenatidine treatment alone. Moreover, similar trend was observed in case of ERK1/2 and JNK1/2 phosphorylation and MMP‐2 expression after the cotreatment. Taken together, the mechanism by which dehydrocrenatidine can decrease the phosphorylation of ERK1/2 and JNK1/2, follow decrease the expression of MMP‐2 and inhibits head and neck cancer cells invasion and migration. This present study identifies dehydrocrenatidine as a potent antimetastatic agent that can be used clinically to improve head and neck cancer prognosis.

CCL3‐CCR5 axis promotes cell migration and invasion of colon adenocarcinoma via Akt signaling pathway

“…Five random fields were captured from each group using a microscope (Nikon, Tokyo, Japan) and cell numbers were counted. For cell migration assay, the procedures were the same as above expect that no Matrigel was precoated in the upper chamber 35–37 …”

“…For cell migration assay, the procedures were the same as above expect that no Matrigel was precoated in the upper chamber. [35][36][37]…”

Bioactive phytocompounds for oral cancer prevention and treatment: A comprehensive and critical evaluation

“…Velmurugan and team 89 studied dehydrocrenatidine in vitro using FaDu, SCC9, and SCC47 cell lines. The investigators found that treatment with dehydrocrenatidine reduced cellular viability, motility, migration, and invasion in all three cell lines.…”

“…Regarding apoptosis, dehydrocrenatidine augmented phosphorylation of p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase 1 (JNK-1) also known as MAPK8, JNK-2 (MAPK9), ERK-1, and ERK-2, and Akt, as well as decreased expression of Fas, Fasassociated death domain protein (FADD), tumor necrosis factor (TNF)-receptor associated death domain protein (TEADD), TNF-receptor 1 (TNFR1), and receptor-interacting protein (RIP) expression. Furthermore, there was an increase in decoy receptor 2 (DcR2) and death receptor 5 (DR5) expression, Bax, Bak, truncated BH3-interacting domain death agonist (tBid) and Bcl-2, as well as a decrease Bcl-2 and B-cell lymphoma-extra-large (Bcl-xL).Velmurugan and team89 studied dehydrocrenatidine in vitro using FaDu, SCC9, and SCC47 cell lines. The investigators found that treatment with dehydrocrenatidine reduced cellular viability, motility, migration, and invasion in all three cell lines.…”

miR-6742-5p regulates the invasion and migration of lung adenocarcinoma cells via mediating FGF8/ERK12/MMP9/MMP2 signaling pathway

“…Moreover, matrix metalloproteinases (MMPs) are key executors of tumor invasion, which are the downstream products of ERK1/2 signals. They inhibit tumor metastasis by degrading the fibrous or stromal tissue surrounding the tumor, thus limiting the cancer cell migration throughout the body [20][21][22][23]. Hence, FGFs, ERK1/2 and MMPs are key checkpoints for cancer suppression.…”