A basal level of phosphorylated STAT3 was present in DRGs of control animals, it remained at a high level up to 6 h after the capsaicin treatment, then markedly decreased and recovered on day 8 and day 16.
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How do primary and metastatic tumors differ in phosphorylation of STAT3?
Stat-3p inhibition is a promising treatment for both inflammation and new bone formation in AS. STAT3 phosphorylation inhibition for treating inflammation and new bone formation in ankylosing spondylitis Rheumatology (Oxford). 2021 Aug 2;60(8):3923-3935. doi: 10.1093/rheumatology/keaa846. ...
Does STAT3 phosphorylation at tyrosine 705 and serine 727 regulate EMT–MET switch?
Dec 01, 2020 · SCDCs were isolated from long bones after for FACS analysis of various cancer cells after MSC-RFP cells injection for 1 and 2 weeks. After MSC-RFP cells injection for 1 week, …
Does peripheral nerve lesion lead to rapid activation of STAT3?
Mar 21, 2022 · After prolonged treatment, differentiated cancer cells are eliminated, however a subpopulation of malignant cells, the cancer stem cells, persist. Upregulation of STAT3 occurs …
Do LIFR and ps727-stat3 levels affect lung cancer survival?
Jul 30, 2020 · We show that LPS does not induce STAT3 phosphorylation on S727 in MyD88 −/ ... ECAR and OCR were measured under basal conditions prior to sequential treatment of cells …
What is metastasis in cancer?
Metastasis, which causes more than 90% of cancer-related deaths, is a multistage process during which malignant cells spread from the primary tumor into distant organs. The “early dissemination” definition was refined by Husemann et al. [ 1] when they found that early disseminated cancer cells (eDCCs) originate at times when lesions are only defined in situ by light microscopy (a clinically latent stage of hidden cancer spread). Cancer of unknown primary is a relatively frequent event in solid cancers where metastases develop without the presence of an obvious primary tumor mass that evolved to become invasive [ 2 ]. In fact, at the time of diagnosis, cancer cell dissemination has occurred in >50% of patients [ 3 ]. In addition, eDCCs detected in patients before the manifestation of cancer metastasis contain fewer genetic abnormalities than primary tumors in breast cancer [ 4 ], pancreatic cancer [ 5 ], and melanoma [ 6] models, indicate that dissemination might occur during the early stages of tumor evolution [ 1 ]. However, the mechanisms that might allow eDCCs to complete all steps of metastasis are unknown.
What is the epithelial mesenchymal transition?
Epithelial–mesenchymal transition (EMT)/mesenchymal–epithelial transition (MET) processes are proposed to be a driving force of cancer metastasis. By studying metastasis in bone marrow-derived mesenchymal stem cell (BM-MSC)-driven lung cancer models, microarray time-series data analysis by systems biology approaches revealed BM-MSC-induced signaling triggers early dissemination of CD133 + /CD83 + cancer stem cells (CSCs) from primary sites shortly after STAT3 activation but promotes proliferation towards secondary sites. The switch from migration to proliferation was regulated by BM-MSC-secreted LIF and activated LIFR/p-ERK/pS727-STAT3 signaling to promote early disseminated cancer cells MET and premetastatic niche formation. Then, tumor-tropic BM-MSCs circulated to primary sites and triggered CD151 + /CD38 + cells acquiring EMT-associated CSC properties through IL6R/pY705-STAT3 signaling to promote tumor initiation and were also attracted by and migrated towards the premetastatic niche. In summary, STAT3 phosphorylation at tyrosine 705 and serine 727 differentially regulates the EMT–MET switch within the distinct molecular subtypes of CSCs to complete the metastatic process.
What is the CSC theory?
The CSC theory posits that CSCs mediate metastasis, are resistant to chemotherapy, and contribute to relapse. Liu et al. demonstrated that breast CSCs can exist in distinct mesenchymal-like (EMT) and epithelial-like (MET) states [ 16 ].