A combined proteomic and metabolomic analysis of the early aborted embryonic tissues with maternal COVID-19 infection.

COVID-19 still spreads worldwide, and repeated infections are hard to avoid. Maternal infection during pregnancy is associated with adverse maternal and neonatal outcomes. Our study used a multi-omics profiling method to explore the proteome and metabolome alteration in early embryonic development after COVID-19 infection.

Syndecan-1 inhibition promotes antitumor immune response and facilitates the efficacy of anti-PD1 checkpoint immunotherapy.

Tumor cell-originated events prevent efficient antitumor immune response and limit the application of anti-PD1 checkpoint immunotherapy. We show that syndecan-1 (SDC1) has a critical role in the regulation of T cell-mediated control of tumor growth. SDC1 inhibition increases the permeation of CD8 T cells into tumors and triggers CD8 T cell-mediated control of tumor growth, accompanied by increased proportions of progenitor-exhausted and effector-like CD8 T cells.

UBXN1 promotes liver tumorigenesis by regulating mitochondrial homeostasis.

Background: The maintenance of mitochondrial homeostasis is critical for tumor initiation and malignant progression because it increases tumor cell survival and growth. The molecular events controlling mitochondrial integrity that facilitate the development of hepatocellular carcinoma (HCC) remain unclear. Here, we report that UBX domain-containing protein 1 (UBXN1) hyperactivation is essential for mitochondrial homeostasis and liver tumorigenesis.

UBXN9 inhibits the RNA exosome function to promote T cell control of liver tumorigenesis.

Background And Aims: Liver tumorigenesis encompasses oncogenic activation and self-adaptation of various biological processes in premalignant hepatocytes to circumvent the pressure of cellular stress and host immune control. Ubiquitin regulatory X domain-containing proteins (UBXNs) participate in the regulation of certain signaling pathways. However, whether UBXN proteins function in the development of liver cancer remains unclear.

Bilateral axillary node calcifications: a case report and revisiting causes.

A 48-year woman was found to have bilateral axillary nodal microcalcifications on screening mammogram; a new finding compared to the prior mammogram done about 8 years ago. Combining the new finding with the amorphous and fine morphology of the microcalcifications, deemed it suspicious. In the absence of a definite benign cause, that could be attributed to this finding, biopsy was performed.

ETV4 potentiates nuclear YAP retention and activities to enhance the progression of hepatocellular carcinoma.

Dysregulation of the Hippo pathway that promotes cell survival, proliferation and tumorigenesis, relays on the coordinated interactions of YAP with the factors that determine YAP translocation and the related transcriptional programming. Here, we demonstrate that ETV4, a transcriptional factor participating in various protumorigenic processes, enhances YAP-mediated transactivation and hepatocellular carcinoma (HCC) progression. Mechanistically, the enhancement of YAP activities is mediated by the interaction between ETV4 and YAP, which not only increases nuclear YAP accumulation but also directly augments the YAP/TEAD4-mediated transcriptional activation in tumor cells.

Comparing the effectiveness of Chinese patent medicines containing red yeast rice on hyperlipidaemia: A network meta-analysis of randomized controlled trials.

Introduction: The purpose of this study was to evaluate the therapeutic effectiveness of Chinese patent medicines containing red yeast rice for the treatment of hyperlipidaemia.

Methods: Relevant literature published until 13 August 2021, was retrieved from six electronic databases. Randomized clinical trials of Chinese patent medicines containing red yeast rice in patients with hyperlipidaemia were included in the review.

USP12 downregulation orchestrates a protumourigenic microenvironment and enhances lung tumour resistance to PD-1 blockade.

Oncogenic activation of KRAS and its surrogates is essential for tumour cell proliferation and survival, as well as for the development of protumourigenic microenvironments. Here, we show that the deubiquitinase USP12 is commonly downregulated in the Kras-driven mouse lung tumour and human non-small cell lung cancer owing to the activation of AKT-mTOR signalling. Downregulation of USP12 promotes lung tumour growth and fosters an immunosuppressive microenvironment with increased macrophage recruitment, hypervascularization, and reduced T cell activation.

Deubiquitination of the repressor E2F6 by USP22 facilitates AKT activation and tumor growth in hepatocellular carcinoma.

Dysregulated ubiquitination of tumor-related proteins plays a critical role in tumor development and progression. The deubiquitinase USP22 is aberrantly expressed in certain types of cancer and contributes to aggressive tumor progression. However, the precise mechanism underlying the pro-tumorigenic function of USP22 in hepatocellular carcinoma (HCC) remains unclear.

The deubiquitinase USP16 functions as an oncogenic factor in K-RAS-driven lung tumorigenesis.

K-RAS mutation and molecular alterations of its surrogates function essentially in lung tumorigenesis and malignant progression. However, it remains elusive how tumor-promoting and deleterious events downstream of K-RAS signaling are coordinated in lung tumorigenesis. Here, we show that USP16, a deubiquitinase involved in various biological processes, functions as a promoter for the development of K-RAS-driven lung tumor.

Effectiveness of tonifying-kidney and regulating-liver therapy on diminished ovarian reserve: a systematic review and Meta-analysis of randomized controlled trials.

Objective: To evaluate the effectiveness of the Traditional Chinese Medicine tonifying-kidney and regulating-liver therapy on diminished ovarian reserve (DOR).

Methods: The literature was comprehensively searched up to August 2019 using four Chinese and three English electronic databases to extract randomized clinical trials (RCTs) comparing Traditional Chinese Medicine tonifying-kidney and regulating-liver prescriptions (combined with hormone therapy or not) with Western Medicine. Data quality evaluation was conducted using the Cochrane risk of bias tool.

POH1 contributes to hyperactivation of TGF-β signaling and facilitates hepatocellular carcinoma metastasis through deubiquitinating TGF-β receptors and caveolin-1.

Background: Hyper-activation of TGF-β signaling is critically involved in progression of hepatocellular carcinoma (HCC). However, the events that contribute to the dysregulation of TGF-β pathway in HCC, especially at the post-translational level, are not well understood.

Methods: Associations of deubiquitinase POH1 with TGF-β signaling activity and the outcomes of HCC patients were examined by data mining of online HCC datasets, immunohistochemistry analyses using human HCC specimens, spearman correlation and survival analyses.

USP1 inhibition destabilizes KPNA2 and suppresses breast cancer metastasis.

Metastatic progression is the main cause of mortality in breast cancer, necessitating the determination of the molecular events driving this process for the development of new therapeutic approaches. Here, we demonstrate that hyperactivation of the deubiquitinase USP1 contributes to breast cancer metastasis. Upregulated USP1 expression in primary breast cancer specimens correlates with metastatic progression and poor prognosis in breast cancer patients.

POH1 deubiquitinates pro-interleukin-1β and restricts inflammasome activity.

Inflammasome activation is essential for host defence against invading pathogens, but is also involved in various forms of inflammatory diseases. The processes that control inflammasome activity are thus important for averting excessive immune responses and tissue damage. Here we show that the deubiquitinase POH1 negatively regulates the immune response triggered by inflammasome activation.

Requirement for POH1 in differentiation and maintenance of regulatory T cells.

Foxp3-expressing regulatory T (Treg) cells are essential for averting autoimmune diseases and maintaining immune homeostasis. However, the molecular mechanisms underlying the development and maintenance of Treg cells are still unclear. Here, we found that T cell-specific deletion of the gene encoding the deubiquitinase POH1 compromised the development of mature T cells, especially CD4Foxp3 Treg cells.

USP16 Downregulation by Carboxyl-terminal Truncated HBx Promotes the Growth of Hepatocellular Carcinoma Cells.

Hepatitis B virus (HBV) infection is a major factor that contributes to the development of hepatocellular carcinoma (HCC). HBV X protein (HBx) has been shown to accelerate HCC progression by promoting tumour growth and metastasis. In the clinic, carboxyl-terminal truncated HBx (Ct-HBx) proteins are frequently present in HCC tumour tissues, but not in non-tumorous tissues.

POH1 deubiquitylates and stabilizes E2F1 to promote tumour formation.

Hyperactivation of the transcriptional factor E2F1 occurs frequently in human cancers and contributes to malignant progression. E2F1 activity is regulated by proteolysis mediated by the ubiquitin-proteasome system. However, the deubiquitylase that controls E2F1 ubiquitylation and stability remains undefined.

SIP1 is a downstream effector of GADD45G in senescence induction and growth inhibition of liver tumor cells.

Cellular senescence evasion caused by the inactivation of tumor suppressive programs is implicated in tumor initiation and therapeutic resistance. Our previous study has shown that the downregulation of growth arrest and DNA damage 45G (GADD45G) contributes to senescence bypass in hepatocellular carcinoma (HCC). Here, we report that the Smad-interacting protein-1 (SIP1) is transcriptionally activated and functions critically in the GADD45G-induced tumor cell senescence.

Association of interleukin-12 gene polymorphisms with cancer susceptibility: a meta-analysis.

Objective: To evaluate the association between interleukin-12 (IL-12) gene polymorphism and cervical cancer susceptibility.

Methods: We comprehensively retrieved the relevant English and Chinese database to collect case-control studies on the association between the IL-12 gene polymorphism and cervical cancer susceptibility. Data were extracted independently by two researchers respectively, the summary data were analyzed using Revman 5.

The expression of CDK1 is associated with proliferation and can be a prognostic factor in epithelial ovarian cancer.

Overexpression of cyclin-dependent kinase 1 (CDK1) has been noted to correlation with several human cancers. However, the effects of CDK1 on ovarian cancer development remain unclear. The aim of this study was to examine the effect of CDK1 and related mechanism in the proliferation and resistance to chemotherapeutic drugs of epithelial ovarian cancer (EOC).

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells.

Background: Kruppel-like factors (KLFs) are involved in various biological processes; emerging studies have indicated that KLF9 plays a critical role in regulating tumorigenesis. The role of KLF9 in prostate cancer (PCa), however, has not yet been investigated.

Methods: The expression of KLF members, AKT- and apoptosis-related proteins were analyzed by Western blot or qRT-PCR.

Chinese herbal medicine Xinfeng Capsule in treatment of rheumatoid arthritis: study protocol of a multicenter randomized controlled trial.

Background: Rheumatoid arthritis (RA), as a common systemic inflammatory autoimmune disease, affects approximately 1 in 100 individuals. Effective treatment for RA is not yet available because current research does not have a clear understanding of the etiology and pathogenesis of RA. Xinfeng Capsule, a patent Chinese herbal medicine, has been used in the treatment of RA in recent years.

AKT hyperactivation confers a Th1 phenotype in thymic Treg cells deficient in TGF-β receptor II signaling.

The generation of CD4⁺Foxp3⁺ Treg cells in the thymus is crucial for immune homeostasis and self-tolerance. Recent studies have shown Treg-cell plasticity when Th-related transcriptional factors and cytokines are present. However, the mechanisms that maintain the stability of Treg cells are poorly understood.