Anoectochilus roxburghii was grown under different shade treatments–50%, 30%, 20%, and 5% of natural irradiance–to evaluate its photosynthetic characteristics, chloroplast ultrastructure, and physiology. The highest net photosynthetic rates and stomatal conductance were observed under 30% irradiance, followed in descending order by 20%, 5%, and 50% treatments. As irradiance decreased from 50% to 30%, electron transport rate and photochemical quenching increased, while non-photochemical quenching indexes declined. Reductions in irradiance significantly increased Chl a and Chl b contents and decreased Chl a/b ratios. Chloroplast ultrastructure generally displayed the best development in leaves subjected to 30% irradiance. Under 50% irradiance, leaf protein content remained relatively stable during the first 20 days of treatment, and then increased rapidly. The highest peroxidase and superoxide dismutase levels, and the lowest catalase activities, were observed in plants subjected to the 50% irradiance treatment. Soluble sugar and malondialdehyde contents were positively correlated with irradiance levels. Modulation of chloroplast development, accomplished by increasing the number of thylakoids and grana containing photosynthetic pigments, is an important shade tolerance mechanism in A. roxburghii.

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Evidence suggests that increased microRNA-155 (miR-155) expression in immune cells enhances anti-tumor immune responses. However, given the reported association of miR-155 to tumorigenesis in various cancers, a debate is provoked on whether miR-155 is oncogenic or tumor suppressive. We aimed to interrogate the impact of tumor miR-155 expression, particularly cancer cell-derived miR-155, on anti-tumor immunity in breast cancer. We performed bioinformatic analysis of human breast cancer databases, murine experiments, and human specimen examination. We revealed that higher tumor miR-155 levels correlate with a favorable anti-tumor immune profile and better patient outcomes.Murine experiments demonstrated that miR-155 overexpression in breast cancer cells enhanced T cell influx, delayed tumor growth, and sensitized the tumors to immune checkpoint blockade (ICB) therapy. Mechanistically, miR-155 overexpression in breast cancer cells upregulated their CXCL9/10/11 production, which was mediated by SOCS1 inhibition and increased pSTAT1/pSTAT3 ratio. We further found that serum miR-155 levels in breast cancer patients correlate with tumor miR-155 levels and tumor immune status. Our findings suggest that high serum and tumor miR-155 levels may be a favorable prognostic marker for breast cancer patients, and therapeutic elevation of miR-155 in breast tumors may improve the efficacy of ICB therapy via remodeling the anti-tumor immune landscape.

Recent scientific evidence has suggested that long noncoding RNAs (lncRNAs) play an important part in tumorigenesis as an important member of competing endogenous RNAs (ceRNAs). Hundreds of RNA sequence data and relevant clinic information are freely accessible in The Cancer Genome Atlas (TCGA) datasets. However, the role of cancer‐related lncRNAs in papillary thyroid cancer (PTC) is not fully understood yet. In this study, we identified 461 RNA sequencing data from TCGA. Subsequently, 45 lncRNAs, 21 miRNAs, and 78 mRNAs were chosen to construct a ceRNA network of PTC. Then, we analyzed the correlation between these 45 PTC‐specific lncRNAs and clinic features and patient outcome. Thirty‐seven of these lncRNAs were found to be closely related to age, race, gender, lymph node metastasis, TNM staging system, and patient outcome. Additionally, three of them were linked to PTC patient overall survival. Eventually, we selected eight lncRNAs randomly and performed quantificational real‐time polymerase chain reaction (qRT‐PCR) in 28 newly diagnosed patients with PTC to verify the reliability of the above results. The results of qRT‐PCR are totally in agreement with the bioinformatics analysis. Additionally, it was found that HAND2‐AS1 was negatively related to tumor size (P < 0.05). The results were consistent with the bioinformatics analysis in TCGA. Taken together, we identified the differentially expressed lncRNAs and constructed a PTC ceRNA network. The study provides a new perspective and supplement for our understanding of lncRNAs in PTC development and reveals potential diagnostic and prognostic markers in PTC.

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