Pengxiang Min
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View article: Multimode neural population coding of diverse innate fear response by mitral and tufted cells
Multimode neural population coding of diverse innate fear response by mitral and tufted cells Open
Neurons that encode odor information are fundamental to innate fear processes, yet how mitral/tufted (M/T) cells encode innate fear remains unknown. Here, we identify three different response patterns of M/T cells in the dorsal olfactory b…
View article: Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation
Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation Open
The poor prognosis of glioblastoma (GBM) patients is attributed mainly to abundant neovascularization and presence of glioblastoma stem cells (GSCs). GSCs are preferentially localized to the perivascular niche to maintain stemness. However…
View article: High MICAL-L2 promotes cancer progression and drug resistance of renal clear cell carcinoma cell via stabilization of ACTN4 and following vimentin expression
High MICAL-L2 promotes cancer progression and drug resistance of renal clear cell carcinoma cell via stabilization of ACTN4 and following vimentin expression Open
Kidney clear cell carcinoma (KIRC) continues to be a substantial contributor to cancer-associated fatalities nowadays. Targeted therapies persist as the conventional method of KIRC treatment. Nevertheless, the development of resistance to …
View article: Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells <i>via</i> regulating β-catenin activation and EMT pathways
Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells <i>via</i> regulating β-catenin activation and EMT pathways Open
Glioblastoma (GBM) is a highly vascularized malignant brain tumor with poor clinical outcomes. Vasculogenic mimicry (VM) formed by aggressive GBM cells is an alternative approach for tumor blood supply and contributes to the failure of ant…
View article: Comprehensive Analysis of MICALL2 Reveals Its Potential Roles in EGFR Stabilization and Ovarian Cancer Cell Invasion
Comprehensive Analysis of MICALL2 Reveals Its Potential Roles in EGFR Stabilization and Ovarian Cancer Cell Invasion Open
Molecules interacting with CasL (MICALs) are critical mediators of cell motility that act by cytoskeleton rearrangement. However, the molecular mechanisms underlying the regulation of cancer cell invasion remain elusive. The aim of this st…
View article: MICAL1 stability by PlexinA1 promotes gastric cancer cell migration
MICAL1 stability by PlexinA1 promotes gastric cancer cell migration Open
Background For metastasis to proceed, tumor cells must become mobile by modulating their cytoskeleton. MICAL1 is known as an actin cytoskeleton regulator, but the mechanisms by which it drives cancer cell migration are still unclear. Metho…
View article: Comprehensive analysis of MICALL2 reveals its potential roles in EGFR stabilization and ovarian cancer cell invasion
Comprehensive analysis of MICALL2 reveals its potential roles in EGFR stabilization and ovarian cancer cell invasion Open
Molecules interacting with CasL (MICALs) are critical mediators of cell motility that act by cytoskeleton rearrangement. However, the molecular mechanisms underlying the regulation of cancer cell invasion remain elusive. The aim of this st…
View article: Striatal CDK5 Regulates Cholinergic Neuron Activation and Dyskinesia-like Behaviors through BK Channels
Striatal CDK5 Regulates Cholinergic Neuron Activation and Dyskinesia-like Behaviors through BK Channels Open
Disturbance of the cholinergic system plays a crucial role in the pathological progression of neurological diseases that cause dyskinesia-like behaviors. However, the molecular mechanisms underlying this disturbance remain elusive. Here, w…
View article: MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway
MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway Open
Background Gastric cancer is a common and lethal human malignancy worldwide and cancer cell metastasis is the leading cause of cancer-related mortality. MICAL2, a flavoprotein monooxygenase, is an important regulator of epithelial-to-mesen…
View article: TGFβ signaling activation correlates with immune-inflamed tumor microenvironment across human cancers and predicts response to immunotherapy
TGFβ signaling activation correlates with immune-inflamed tumor microenvironment across human cancers and predicts response to immunotherapy Open
Considering the determining role of TGFβ signaling in the tumor microenvironment (TME) on immune evasion, the inhibition of signaling is expected to enhance the therapeutic efficacy of immunotherapies, especially immune checkpoint blockade…
View article: MICAL2 contributes to gastric cancer cell migration via Cdc42- dependent activation of E‑cadherin/β-catenin signaling pathway
MICAL2 contributes to gastric cancer cell migration via Cdc42- dependent activation of E‑cadherin/β-catenin signaling pathway Open
Background Gastric cancer is a common and lethal human malignancy worldwide and cancer cell metastasis is the leading cause of cancer-related mortality. MICAL2, a flavoprotein monooxygenase, is an important regulator of epithelial-to-mesen…
View article: TGFβ signaling activation correlates with immune-inflamed tumor microenvironment across human cancers and predicts response to immunotherapy
TGFβ signaling activation correlates with immune-inflamed tumor microenvironment across human cancers and predicts response to immunotherapy Open
Considering the determining role of TGFβ signaling in the tumor microenvironment (TME) on immune evasion, the inhibition of signaling is expected to enhance the therapeutic efficacy of immunotherapies, especially immune checkpoint blockade…
View article: MICAL2 Facilitates Gastric Cancer Cell Migration via MRTF-A-Mediated CDC42 Activation
MICAL2 Facilitates Gastric Cancer Cell Migration via MRTF-A-Mediated CDC42 Activation Open
Aims and Hypothesis: Cell migration is driven by the reorganization of the actin cytoskeleton. Although MICAL2 is known to mediate the oxidation of actin filaments to regulate F-actin dynamics, relatively few studies have investigated the …
View article: MICAL-L2 Is Essential for c-Myc Deubiquitination and Stability in Non-small Cell Lung Cancer Cells
MICAL-L2 Is Essential for c-Myc Deubiquitination and Stability in Non-small Cell Lung Cancer Cells Open
Objectives: MICAL-L2, a member of the molecules interacting with the CasL (MICAL) family, was reported to be highly expressed in several types of cancers, however, the roles of MICAL-L2 in NSCLC pathogenesis remain to be explored. This stu…
View article: MICAL2 Contributes to Gastric Cancer Cell Proliferation by Promoting YAP Dephosphorylation and Nuclear Translocation
MICAL2 Contributes to Gastric Cancer Cell Proliferation by Promoting YAP Dephosphorylation and Nuclear Translocation Open
Dynamic cytoskeletal rearrangements underlie the changes that occur during cell division in proliferating cells. MICAL2 has been reported to possess reactive oxygen species‐ (ROS‐) generating properties and act as an important regulator of…
View article: FLCN Regulates HIF2α Nuclear Import and Proliferation of Clear Cell Renal Cell Carcinoma
FLCN Regulates HIF2α Nuclear Import and Proliferation of Clear Cell Renal Cell Carcinoma Open
Aims and Hypothesis: This study aims to explore the specific molecular mechanism of folliculin (FLCN)-induced proliferation, migration, and invasion in clear cell renal cell carcinoma (ccRCC) and to investigate the relationship of F…
View article: mTORC2 mediate FLCN-induced HIF2α nuclear import and proliferation of clear cell renal cell carcinoma
mTORC2 mediate FLCN-induced HIF2α nuclear import and proliferation of clear cell renal cell carcinoma Open
Clear cell renal cell carcinoma (ccRCC), as the most important type of renal carcinoma, has a high incidence and easy metastasis. Folliculin (FLCN) was identified as a tumor suppressor gene. Its deletions and mutations are associated with …
View article: SOX2 promotes hypoxia-induced breast cancer cell migration by inducing NEDD9 expression and subsequent activation of Rac1/HIF-1α signaling
SOX2 promotes hypoxia-induced breast cancer cell migration by inducing NEDD9 expression and subsequent activation of Rac1/HIF-1α signaling Open
View article: MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration
MICAL‐L2 potentiates Cdc42‐dependent EGFR stability and promotes gastric cancer cell migration Open
Enhanced migration potential is a common characteristic of cancer cells induced by mechanisms that are incompletely defined. The present study was designed to investigate relationship of a new discovered cytoskeleton regulator MICAL‐L2 and…
View article: Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway Open
Tumor cell migration is a critical step in cancer metastasis. Over-activated Notch pathway can promote the migration of cancer cells, especially in the breast cancer. However, the underlying mechanism of non-canonical Notch signaling in mo…
View article: NEDD9 Facilitates Hypoxia-Induced Gastric Cancer Cell Migration via MICAL1 Related Rac1 Activation
NEDD9 Facilitates Hypoxia-Induced Gastric Cancer Cell Migration via MICAL1 Related Rac1 Activation Open
In all, it is concluded that MICAL1 is regulated by NEDD9 that facilitates hypoxia-induced gastric cancer cell migration via Rac1-dependent manner.
View article: COX-2 expression correlation with invasion in human breast carcinomas and in cell line MDA-MB-231 in vitro
COX-2 expression correlation with invasion in human breast carcinomas and in cell line MDA-MB-231 in vitro Open
COX-2 expression by means of immunohistochemistry in 120 cases breast invasive ductal carcinomas and 60 cases benign lesions were compared with clinicopathological features and prognostic molecular markers. COX-2 role of invasiveness and c…