Key message
Carbon stock density was quite similar in planted vs natural forest of Masson’s pine (
Pinus massoniana
Lamb.) in China across three ages (7, 15, and 50 years). The stock in the standing ...trees was larger in planted than in natural forests, but this difference was compensated by larger stocks in the soil and the debris of natural forests.
Context
Most studies on the carbon stocks are focused on management strategies to maximize carbon stocks. We still lack data comparing planted vs natural conifer forests.
Aims
We compared carbon storage in the different compartment (vegetation, soil, debris) along a chronosequence of Masson’s pine plantations vs natural forests.
Methods
We investigated 58 Masson’s pine (
Pinus massoniana
Lamb.) forest stands (20 m × 50 m plots), that differ in stand management (planted and natural forests) and age (young, middle-aged, and mature ages) and then calculated the carbon stock densities of vegetation biomass (tree, shrub, and herb), debris, and soil.
Results
The carbon stock densities in the planted and natural Masson’s pine forest ecosystems ranged from 78 to 210 Mg ha
−1
and from 97 to 177 Mg ha
−1
respectively. The carbon stock densities in the vegetation were significantly greater in planted forests than in natural forests. A lower carbon stock density in debris and soil alleviated the increase of biomass carbon stock densities in planted vs natural forests, leading to similar carbon stock densities at ecosystem level. The carbon stock densities in the vegetation increased with age, whereas those of debris and soil remained stable.
Conclusions
Planted forests of Masson’s pine sequester similiar amounts of carbon at ecosystem level to those in natural forests, reinforcing the idea that planted pine forests can contribute to the mitigation of greenhouse gas emission.
Malignant glioblastoma multiforme (GBM) is an aggressive brain tumor with strong local invasive growth and a poor prognosis. One probable way to manipulate GBM cells toward a less invasive status is ...to reprogram the most malignant GBM cells to a more differentiated and less oncogenic phenotype. Herein, we identified a novel role of a RING finger protein Znf179 in gliomagenesis. Znf179 overexpression induced differentiation of primary GBM cells, which were accompanied with elevated glial fibrillary acidic protein (GFAP) expression through up-regulating several cell-cycle-related factors, p53, p21, and p27, and allowed the cell-cycle arrest in the G
/G
phase. In addition, Znf179 was highly correlated with the prognosis and survival rates of glioma patients. The expression levels of Znf179 was relatively lower in glioma patients compared to normal people, and glioma patients with lower expression levels of Znf179 mRNA had poorer prognosis and lower survival rates. In conclusion, we provide novel insight that Znf179 can reprogram GBM cells into a more-differentiated phenotype and prevent the progression of gliomas to a more-malignant state through p53-mediated cell-cycle signaling pathways. Understanding the molecular mechanism of Znf179 in gliomagenesis could help predict prognostic consequences, and targeting Znf179 could be a potential biomarker for glioma progression.
Nectin-4 is a novel biomarker overexpressed in various types of cancer, including breast cancer, in which it has been associated with poor prognosis. Current literature suggests that nectin-4 has a ...role in cancer progression and may have prognostic and therapeutic implications. The present study aims to produce nectin-4-specific single-chain variable fragment (scFv) antibodies and evaluate their applications in breast cancer cell lines and clinical specimens.
We generated recombinant nectin-4 ectodomain fragments as immunogens to immunize chickens and the chickens' immunoglobulin genes were amplified for construction of anti-nectin-4 scFv libraries using phage display. The binding capacities of the selected clones were evaluated with the recombinant nectin-4 fragments, breast cancer cell lines, and paraffin-embedded tissue sections using various laboratory approaches. The binding affinity and
docking profile were also characterized.
We have selected two clones (S21 and L4) from the libraries with superior binding capacity. S21 yielded higher signals when used as the primry antibody for western blot analysis and flow cytometry, whereas clone L4 generated cleaner and stronger signals in immunofluorescence and immunohistochemistry staining. In addition, both scFvs could diminish attachment-free cell aggregation of nectin-4-positive breast cancer cells. As results from ELISA indicated that L4 bound more efficiently to fixed nectin-4 ectodomain, molecular docking analysis was further performed and demonstrated that L4 possesses multiple polar contacts with nectin-4 and diversity in interacting residues.
Overall, the nectin-4-specific scFvs could recognize nectin-4 expressed by breast cancer cells and have the merit of being further explored for potential diagnostic and therapeutic applications.
The expression of cancer stemness is believed to reduce the efficacy of current therapies against hepatocellular carcinoma (HCC). Understanding of the stemness-regulating signaling pathways incurred ...by a specific etiology can facilitate the development of novel targets for individualized therapy against HCC. Niche environments, such as virus-induced inflammation, may play a crucial role. However, the mechanisms linking inflammation and stemness expression in HCC remain unclear. Here we demonstrated the distinct role of inflammatory mediators in expressions of stemness-related properties involving the pluripotent octamer-binding transcription factor 4 (OCT4) in cell migration and drug resistance of hepatitis B virus-related HCC (HBV-HCC). We observed positive immunorecognition for macrophage chemoattractant protein 1 (MCP-1)/CD68 and OCT4/NANOG in HBV-HCC tissues. The inflammation-conditioned medium (inflamed-CM) generated by lipopolysaccharide-stimulated U937 human leukemia cells significantly increased the mRNA and protein levels of OCT4/NANOG preferentially in HBV-active (HBV+HBsAg+) HCC cells. The inflamed-CM also increased the side population (SP) cell percentage, green fluorescent protein (GFP)-positive cell population, and luciferase activity of OCT4 promoter-GFP/luciferase in HBV-active HCC cells. Furthermore, the inflamed-CM upregulated the expressions of insulin-like growth factor-I (IGF-I)/IGF-I receptor (IGF-IR) and activated IGF-IR/Akt signaling in HBV-HCC. The IGF-IR phosphorylation inhibitor picropodophyllin (PPP) suppressed inflamed-CM-induced OCT4 and NANOG levels in HBV+HBsAg+ Hep3B cells. Forced expression of OCT4 significantly increased the secondary sphere formation and cell migration, and reduced susceptibility of HBV-HCC cells to cisplatin, bleomycin, and doxorubicin. Taking together, our results show that niche inflammatory mediators play critical roles in inducing the expression of stemness-related properties involving IGF-IR activation, and the upregulation of OCT4 contributes to cancer migration and drug resistance of HBV-HCC cells. Findings in this paper would provide potential targets for a therapeutic strategy targeting on inflammatory environment for HBV-HCC.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background
Full‐thickness local excision (FTLE) for rectal cancer showing clinical complete remission (cCR) after neoadjuvant chemoradiation therapy (NCRT) is associated with good oncological ...results. The purpose of this study was to report the results of robotic transanal minimally invasive surgery for such patients.
Methods
Patients were treated with a 5‐fluorouracil‐based NCRT regimen. The determination of cCR was based on digital rectal examination, colonoscopy, and magnetic resonance imaging.
Results
Six patients underwent transanal FTLE using the da Vinci Xi surgical system. The median operative time was 106.5 minutes, and the estimated blood loss was minimal. The mean length of hospital stay was 4.2 days. After 18.2 months of follow‐up, none of the patients developed local recurrences or distant disease.
Conclusions
With the use of robotic technology, FTLE can be performed with relative ease and can be considered as a viable alternative to radical resection or a “Watch and Wait” strategy.
Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical ...significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation.
Cancer progression is influenced by junctional adhesion molecule (JAM) family members. The relationship between JAM family members and different types of cancer was examined using The Cancer Genome ...Atlas dataset. mRNA levels of the F11R (F11 receptor) in tumours were inversely correlated to the expression of JAM‐2 and JAM‐3. This relationship was unique to breast cancer (BCa) and was associated with poor prognosis (p = 0.024, hazard ratio = 1.44 1.05–1.99). A 50‐gene molecular signature (prediction analysis of microarray 50) was used to subtype BCa. F11R mRNA expression significantly increased in human epidermal growth factor receptor 2 (HER2)‐enriched (p = 0.0035) and basal‐like BCa tumours (p = 0.0005). We evaluated F11R protein levels in two different compositions of BCa subtype patient tissue array cohorts to determine the relationship between BCa subtype and prognosis. Immunohistochemistry staining revealed that a high F11R protein level was associated with poor overall survival (p < 0.001; Taipei Medical University TMU cohort, p < 0.001; Kaohsiung Veterans General Hospital KVGH cohort) or disease‐free survival (p < 0.001 TMU cohort, p = 0.034 KVGH cohort) in patients with BCa. Comparison of F11R levels in different subtypes revealed the association of poor prognosis with high levels of F11R among luminal (p < 0.001 TMU cohort, p = 0.027 KVGH cohort), HER2 positive (p = 0.018 TMU cohort, p = 0.037 KVGH cohort), and triple‐negative (p = 0.013 TMU cohort, p = 0.037 KVGH cohort) BCa. F11R‐based RNA microarray analysis and Ingenuity Pathway Analysis were successful in profiling the detailed gene ontology of triple‐negative BCa cells regulated by F11R. The EP300 transcription factor was highly correlated with F11R in BCa (R = 0.51, p < 0.001). By analysing these F11R‐affected molecules with the L1000CDs datasets, we were able to predict some repurposing drugs for potential application in F11R‐positive BCa treatment.
Abstract
Glioblastoma (GBM) is a fatal cancer. Existing therapies do not have significant efficacy for GBM patients. Previous studies have shown that the collagen family is involved in the regulation ...of the extracellular environment of cancer cells, and these conditions could become an important factor for effective treatment. Therefore, we screened various collagen types and observed that the type V collagen α1 chain (COL5A1) gene plays a pivotal role in GBM. We further examined whether the overexpression of COL5A1 is common in mesenchymal subtypes and is related to the survival rate of GBM patients through several in silico cohorts. In addition, our cohort also showed a consistent trend in COL5A1 protein levels. Most importantly, we validated the cell mobility, metastatic ability and actin polymerization status caused by COL5A1 with two-way models. Based on these results, we established a transcriptomics dataset based on COL5A1. Moreover, PPRC1, GK and ESM1 were predicted by ingenuity pathway analysis (IPA) to be transcription factors or to participate downstream. We investigated the involvement of COL5A1 in extracellular remodeling and the regulation of actin filaments in the metastasis of GBM. Our results indicate that the COL5A1−PPRC1−ESM1 axis may represent a novel therapeutic target in GBM.
Endocan (or called Esm-1) has been shown to have tumorigenic activities and its expression is associated with poor prognosis in various cancers. Latent membrane protein 1 (LMP1) is an Epstein-Barr ...virus (EBV)-encoded oncoprotein and has been shown to play an important role in the pathogenesis of EBV-associated nasopharyngeal carcinoma (NPC). To further understand the role of LMP1 in the pathogenesis of NPC, microarray analysis of LMP1-regulated genes in epithelial cells was performed. We found that endocan was one of the major cellular genes upregulated by LMP1. This induction of endocan by LMP1 was confirmed in several epithelial cell lines including an NPC cell line. Upregulation of endocan by LMP1 was found to be mediated through the CTAR1 and CTAR2 domains of LMP1 and through the LMP1-activated NF-κB, MEK-ERK and JNK signaling pathways. To study whether endocan was expressed in NPC and whether endocan expression was associated with LMP1 expression in NPC, the expression of endocan and LMP1 in tumor tissues from 42 NPC patients was evaluated by immunohistochemistry. Expression of endocan was found in 52% of NPC specimens. Significant correlation between LMP1 and endocan expression was observed (p<0.0001). Moreover, NPC patients with endocan expression were found to have a shorter survival than NPC patients without endocan expression (p=0.0104, log-rank test). Univariate and Multivariate analyses revealed that endocan was a potential prognostic factor for NPC. Finally, we demonstrated that endocan could stimulate the migration and invasion ability of endothelial cells and this activity of endocan was dependent on the glycan moiety and the phenylalanine-rich region of endocan. Together, these studies not only identify a new molecular marker that may predict the survival of NPC patients but also provide a new insight to the pathogenesis of NPC.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
•An allelochemical cyclic dipeptide was found in monospecific Chinese fir plantations.•Replanting increases soil allelochemical and pathogenic fungi but reduces root biomass.•Cyclic dipeptide has ...negative correlations with soil microbe and root biomass.•Allelochemical context alters soil microbial community and contributes to replant problem.
Productivity decline of monospecific forest plantations has remained a serious problem. Despite increasing knowledge of the problem involved in the build-up of soil-borne pathogens and allelopathy, relatively little is known about tree-derived allelochemicals and their impacts on the soil microbial community and root growth. Therefore, the objective of this study was to examine a novel allelochemical cyclic dipeptide in relation to the soil microbial community and phytotoxicity to tree roots in 25-year-old monospecific Chinese fir (Cunninghamia lanceolata) forest plantations. We sampled soils and fine roots in situ and quantified soil cyclic dipeptide, microbial and root characteristics along with their correlation analyses. When compared with soil from a plantation established following removal of natural forest vegetation, soil from a replanted plantation contained a greater amount of cyclic dipeptide. Furthermore, increased soil potentially pathogenic fungi and reduced root biomass, root surface area and root length density were observed in the replanted plantations. There were negative relationships among cyclic dipeptide concentration, microbial community composition and root biomass in given plantations. Phospholipid fatty acid profiling showed that the signature lipid biomarkers of soil bacteria and fungi, and soil microbial community structure were affected under cyclic dipeptide application. Soil degradation dynamics indicated that cyclic dipeptide declined rapidly. The results demonstrated that allelochemical cyclic dipeptide not only had direct phytotoxicity to tree roots but also indirectly altered soil microbial community compositions, suggesting that productivity decline of continuous Chinese fir monocultures may be a negative feedback interaction between allelochemical-mediated soil microbial community and root phytotoxicity.
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