EGFR‐mediated matrix metalloproteinase‐7 up‐regulation promotes epithelial‐mesenchymal transition<i>via</i>ERK1‐AP1 axis during ovarian endometriosis progression

Chatterjee, Kasturi; Jana, Sayantan; DasMahapatra, Pramathes; Swarnakar, Snehasikta

doi:10.1096/fj.201701382rr

Cited by 46 publications

(33 citation statements)

References 34 publications

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“…The abated adherence function contributes to the invasion and metastasis of solid tumors (19), and it is accompanied by the weakened expression of E-cadherin and reinforced expression of vimentin (17). The latest investigations demonstrated that MMPs (MMP-2, MMP-7 and MMP-9) play a significant role in EMT in tumors (20)(21)(22)(23)(24). However, the relationship between MMP-1 and EMT is still unexplored.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MMP‑1 inhibits the progression of colorectal cancer by suppressing the PI3K/Akt/c‑myc signaling pathway and EMT

Wang

Zheng

et al. 2020

Oncol Rep

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The present study aimed to investigate the role of matrix metalloproteinase-1 (MMP-1) in the development of colorectal cancer and reveal the mechanism underlying this progression. Bioinformatics methods and a public dataset were first used to analyze MMP-1 gene expression in a public dataset. MMP-1 expression in colorectal cancer patients was assessed by immunohistochemistry; its association with clinicopathological parameters and its significance for prognosis were analyzed. Then proliferation, scratch and Transwell assays and a xenograft model were used to assess the change in malignant behavior in cells transfected with an MMP-1 shRNA. Changes involved in epithelial-mesenchymal transition (EMT) and the Akt signaling pathway were detected by western blotting. According to the results, MMP-1 expression was higher in colorectal cancer tissues than it was in matched adjacent noncancerous tissues, and its high expression was significantly related to lymphatic metastasis as well as TNM stage (P<0.05). Downregulation of MMP-1 expression inhibited the progression of colorectal cancer in vitro and in vivo. Furthermore, after the cells were stably transfected with MMP-1 shRNA, the expression of N-cadherin, vimentin and Twist1 decreased while that of E-cadherin increased. The expression of p-Akt and c-Myc also decreased. In conclusion, MMP-1 may promote malignant behavior in colorectal cancer via EMT and the Akt signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Knockdown of MMP‑1 inhibits the progression of colorectal cancer by suppressing the PI3K/Akt/c‑myc signaling pathway and EMT

Wang

Zheng

et al. 2020

Oncol Rep

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“…The epithelial‐mesenchymal transition (EMT) is an evolutionary conserved biologic process that is crucial for the initiation of metastasis. The loss of E‐cadherin and gain of vimentin expression is a hallmark of the EMT process (3). Many signaling molecules can trigger the EMT process, including TGF‐β, epidermal growth factor, fibroblast growth factor, wingless‐integrated (Wnt)/β‐catenin , and matrix metalloproteinases (MMPs) .…”

mentioning

confidence: 99%

“…miR-214 is located at an intron of the dynamin-3 gene in 1q24. 3. Increasing evidence has shown that miR-214 plays key roles in tumor cell growth, invasiveness, metastasis, chemotherapeutic resistance, angiogenesis, and microenvironment.…”

mentioning

confidence: 99%

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun

Liu²,

Lin

et al. 2019

FASEB j.

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The epithelial‐mesenchymal transition (EMT) is crucial for cancer progression. Evidence has shown that miR‐22 and miR‐214 play a key role in colon cancer progression; however, the underlying mechanism remains to be known. The effects of miR‐22 and miR‐214 on EMT are contradictory in different cancers, and whether miR‐22 and miR‐214 are involved in the colon cancer EMT process needs to be elucidated. In this study, we evaluated the exact role and the regulation mechanism of miR‐22 and miR‐214 in colon cancer. After transfection with miR‐22 expression vector, the cell proliferation and migration capacity of HCT116 and RKO cells were significantly suppressed. Also, E‐cadherin was increased and vimentin was decreased by miR‐22 overexpression. Similar effects were also observed after miR‐214 expression vector transfection. Dual‐lucif erase reporter confirmed that BCL9L is the target gene of both miR‐22 and miR‐214. Silencing of BCL9L inhibits cell proliferation and migration, and the expression of E‐cadherin and vimentin was also altered by BCL9L knockdown, which was consistent with miR‐22 or miR‐214 transfection. Furthermore, miR‐22 and miR‐214 inhibited tumor growth in nude mice. Moreover, although the association between BCL9L's lower expression and longer survival time was statistically nonsignificant, a trend existed; further studies in a larger cohort are needed. Collectively, these data suggest that miR‐22 and miR‐214 inhibit cell proliferation, migration, and EMT of colon cancer, most likely by targeting BCL9L.—Sun, R., Liu, Z., Han, L., Yang, Y., Wu, F., Jiang, Q., Zhang, H., Ma, R., Miao, J., He, K., Wang, X., Zhou, D., Huang, C. miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signliang in colon cancer. FASEB J. 33, 5411–5424 (2019). http://www.fasebj.org

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“…In a study expression of c-Fos and c-Jun in breast tumor samples was significantly lower than adjacent non-tumor tissues [65]. The reduction of these two genes would be related to apoptotic effects of AP1 complex [66,67]. JNK (MAPK8) showed a total reducing trend from N>M in the first dataset while p38 (MAPK14) did not show a considerable change.…”

Section: Ros Promotes the Erk1 Activation And This Activation Increasmentioning

confidence: 96%

“…JNK is also activated by ROS which enhances c-Jun activation another component of AP1 [66]. AP1 complex enters the nucleus and activates expression of genes promoting cell proliferation [67]. The expression level for c-Fos (FOS) reduced in both datasets.…”

Section: Ros Promotes the Erk1 Activation And This Activation Increasmentioning

confidence: 99%

Gene Expression Signature and Molecular Mechanism of Redox Homeostasis in Colorectal Cancer

Piran

Darayee

Piran

et al. 2020

Preprint

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Cellular redox homeostasis is the important tool for normal cell function and survival. Oxidants, reductants and antioxidants are the players to maintain cellular homeostasis balance. However, in some conditions like cancer, the concentration and activation of these players are disturbed.This study walks you through the molecular mechanism of redox homeostasis to describe how expression level of these players would help colorectal cancer (CRC) cells continue proliferation and survive in the hypoxic environment of tumor. We proposed that O2concentration is not detrimentally high in CRC cells since expression level of MnSOD didn't change noticeably. We also suggested that High proliferative CRC cells obtain their energy by oxidation of H2S in or Electron transport chain (ETC) and keep the adequate concentration of H2S by diminishing the expression level of enzymes involved in sulfide oxidation pathway. Reduction in hydrogen sulfide oxidation results in a decrease in the level of GSH. Glutathione peroxidase enzyme requires GSH to convert H2O2 into oxygen and water. Therefore, Level of hydrogen peroxide stays high which leads to an increase in cell proliferation. Furthermore, we analyzed the expression level of transcription factors sensitive to redox messengers. to cell proliferation while a severe increment and long-lasting in the concentration of these molecules causes cell death. As a result, if redox homeostasis is disturbed, oxidative stress contributes to aberrant cell growth/death and disease [2]. This happens by changes in cells environment and impaired antioxidants generation which modulate the concentration of oxidants [5]. ROS includes radical species such as superoxide (O2 -), hydroxyl radical ( . OH) and non-radical species like Hydrogen peroxide (H2O2). RNS involves nitric oxide (NO) and Peroxynitrite (ONOO -) [2, 6]. Moreover, there are two types of antioxidants, enzymatic and non-enzymatic (small molecules). SODs (Superoxide dismutase), Glutathione peroxidase (GPx) and Catalase are examples of enzymatic antioxidants but Glutathione (GSH), Thioredoxin (Tnx) and Peroxiredoxin (Prx) are examples of small molecule antioxidants. One of the primary ROS molecules is O2made in the ETC by transferring electrons from complex one and Three to a dioxygen molecule or by NAD(P)H oxidases (NOX) activation [7-10]. Superoxide is then converted into hydrogen peroxide using Superoxide dismutase enzymes [9]. Among the three kinds of SODs, SOD1 (CuZnSOD) is present in the cytoplasm, mitochondrial inter-membrane space, nucleus, and lysosomes while SOD2 (MnSOD) and SOD3 (Ec-SOD) are present in Mitochondria and Extra Cellular Matrix (ECM) respectively [2]. Next, H2O2 is turned into water and oxygen molecules by GPx enzyme which oxidizes reduced Glutathione (GSH) into oxidized glutathione (GSSG) [11]. GSSG is converted into GSH by Glutathione reductase (GR/GSR) and in the meantime, an NADPH is turned into NADP + . GSH can enter the oxidation cycle again and NADP + enters the glycolysis to be reduced into NADPH [12]. In the p...

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EGFR‐mediated matrix metalloproteinase‐7 up‐regulation promotes epithelial‐mesenchymal transitionviaERK1‐AP1 axis during ovarian endometriosis progression

Cited by 46 publications

References 34 publications

Knockdown of MMP‑1 inhibits the progression of colorectal cancer by suppressing the PI3K/Akt/c‑myc signaling pathway and EMT

Knockdown of MMP‑1 inhibits the progression of colorectal cancer by suppressing the PI3K/Akt/c‑myc signaling pathway and EMT

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Gene Expression Signature and Molecular Mechanism of Redox Homeostasis in Colorectal Cancer

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