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Upregulated Vav2 signaling promotes regenerative proliferation in squamous cell carcinoma

ABSTRACT: Upregulated Vav2 signaling promotes regenerative proliferation in squamous cell carcinoma

PROVIDER: PRJNA510584 | ENA |

REPOSITORIES: ENA

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Upregulated Vav2 signaling promotes regenerative proliferation in squamous cell carcinoma

Project description:Upregulated Vav2 signaling promotes regenerative proliferation in squamous cell carcinoma

| PRJNA510584 | ENA

Upregulated Vav2 signaling promotes regenerative proliferation in squamous cell carcinoma

Project description:Stem cell-like regenerative proliferation and undifferentiation cause poor prognosis in squamous cell carcinoma (SCC). Despite this, the signaling events driving to those traits remain ill-characterized. We report here that VAV2, an enzyme involved in RHO GTPase activation, becomes frequently upregulated in cutaneous and head-and-neck SCC, where it orchestrates a stem cell-like regenerative state.

2020-08-13 | GSE124019 | GEO

Ruxolitinib inhibits Cyclosporine-induced proliferation of cutaneous squamous cell carcinoma

Project description:Ruxolitinib inhibits Cyclosporine-induced proliferation of cutaneous squamous cell carcinoma

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Upregulated Vav2 signaling induces a transcriptomic rewiring in epidermal stem cells

Project description:Upregulated Vav2 signaling induces a transcriptomic rewiring in epidermal stem cells

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Ruxolitinib inhibits Cyclosporine-induced proliferation of cutaneous squamous cell carcinoma

Project description:Organ transplant recipients (OTRs) on Cyclosporine A (CSA) are prone to catastrophic cutaneous squamous cell carcinoma (SCC). Allograft-sparing, cancer-targeting systemic treatments are unavailable. We have shown increased risk for catastrophic SCC in OTRs via CSA-mediated induction of Interleukin-22 (IL-22). Herein, we found CSA drives SCC proliferation and tumor growth through IL-22 and JAK/STAT pathway induction. We in turn inhibited SCC growth with an FDA-approved JAK 1/2 inhibitor, Ruxolitinib. In human SCC cells, greatest proliferative response to IL-22 and CSA treatment occurred in non-metastasizing lines. IL-22 treatment upregulated JAK1 and STAT1/3 in A431 SCC cells. JAK/STAT pathway genes were highly expressed in tumors from a cohort of CSA-exposed OTRs, and in SCC with high risk for metastasis. Compared to immunocompetent SCC, genes associated with innate immunity, response to DNA damage and p53 regulation were differentially expressed in SCC from OTRs. In nude mice engrafted with human A431 cells, IL-22 and CSA treatment increased tumor growth and upregulated IL-22 receptor, JAK1 and STAT 1/3 expression. Ruxolitinib treatment significantly reduced tumor volume and reversed the accelerated tumor growth. CSA and IL-22 exacerbate aggressive behavior in SCC. Targeting the IL-22 axis via selective JAK/STAT inhibition may reduce the progression of aggressive SCC in OTRs, without compromising immunosuppression. In this study, microarray data was used to compare normal skin to immunocompetent SCC, to transplant associated SCC (TSCC)

2018-07-18 | GSE117247 | GEO

CD271 is preferentially expressed and essential for cell proliferation in squamous cell carcinoma of the lung

Project description:Squamous cell carcinoma is a major type of cancer in the lung. While several therapeutic target molecules for lung adenocarcinoma have been identified, little is known about lung squamous cell carcinoma (LSCC). We recently reported that CD271 (p75 neurotrophin receptor) serves as a marker for tumor initiation and is a key regulator of cell proliferation in hypopharyngeal squamous cell carcinoma. In this study, we found that CD271 was also expressed in squamous cell carcinoma, but not in adenocarcinoma, of several tissues, including the lung. To examine CD271’s role in LSCC, we established xenograft cell lines from LSCC patients. Within the sorted live LSCC cell population, the CD271high cells were primarily cycling through the G2/M phase, while the CD271low cells were mostly in the G0 phase. CD271 knockdown in the LSCC cells completely suppressed their proliferation and tumor-formation capability, and increased their cell-cycle arrest in the G0 phase. In the CD271-knockdown cells, ERK-phosphorylation was decreased, while no change was observed in the IκBα-, p65-, or Akt-phosphorylation. Treatment with the MEK inhibitor U0126 decreased the LSCC cells’ proliferation capability. Microarray analysis revealed that CD271 knockdown attenuated the RAS-related pathways. The knockdown of TrkB, which forms a heterodimer with CD271 and accelerates its downstream signaling, partially inhibited the LSCC cell proliferation. These results indicated that LSCC exclusively depends on CD271 for cell proliferation, in part through ERK-signaling activation.

2021-08-06 | GSE118141 | GEO

Quantitative proteomic profiling lung squamous carcinoma cells

Project description:Quantitative proteomic profiling the lung squamous carcinoma cells

2016-07-14 | MSV000079911 | MassIVE

Circular RNA has_circ_0067934 is upregulated in esophageal squamous cell carcinoma and promoted proliferation.

Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent and deadly types of cancer worldwide especially in Eastern Asia and the prognosis of ESCC remain poor. Recent evidence suggests that circular RNAs (circRNAs) play important roles in multiple diseases, including cancer. In this study, we characterized a novel circRNA termed hsa_circ_0067934 in ESCC tumor tissues and cell lines. We analyzed a cohort of 51 patients and found that hsa_circ_0067934 was significantly overexpressed in ESCC tissues compared with paired adjacent normal tissues. The high expression level of hsa_circ_0067934 was associated with poor differentiation (P?=?0.025), I-II T stage (P?=?0.04), and I-II TNM stage (P?=?0.021). The in vitro silence of hsa_circ_0067934 by siRNA inhibited the proliferation and migration of ESCC cells and blocked cell cycle progression. Cell fraction analyses and fluorescence in situ hybridization detected that hsa_circ_0067934 was mostly located in the cytoplasm. Our findings suggest that hsa_circ_0067934 is upregulated in ESCC tumor tissue. Our data suggest that hsa_circ_0067934 represents a novel potential biomarker and therapeutic target of ESCC.

| S-EPMC5067712 | biostudies-literature

Hippo pathway induces PIEZO1 expression to promote oral squamous cell carcinoma cell proliferation

Project description:Hippo pathway induces PIEZO1 expression to promote oral squamous cell carcinoma cell proliferation

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VAV2 signaling promotes regenerative proliferation in both cutaneous and head and neck squamous cell carcinoma.

Project description:Regenerative proliferation capacity and poor differentiation are histological features usually linked to poor prognosis in head and neck squamous cell carcinoma (hnSCC). However, the pathways that regulate them remain ill-characterized. Here, we show that those traits can be triggered by the RHO GTPase activator VAV2 in keratinocytes present in the skin and oral mucosa. VAV2 is also required to maintain those traits in hnSCC patient-derived cells. This function, which is both catalysis- and RHO GTPase-dependent, is mediated by c-Myc- and YAP/TAZ-dependent transcriptomal programs associated with regenerative proliferation and cell undifferentiation, respectively. High levels of VAV2 transcripts and VAV2-regulated gene signatures are both associated with poor hnSCC patient prognosis. These results unveil a druggable pathway linked to the malignancy of specific SCC subtypes.

| S-EPMC7508832 | biostudies-literature

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