Research progress of lncRNA and miRNA in hepatic ischemia-reperfusion injury.

BACKGROUND: Hepatic ischemia-reperfusion injury (HIRI) is a common complication of liver surgeries, such as hepatectomy and liver transplantation. In recent years, several non-coding RNAs (ncRNAs) including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as factors involved in the pathological progression of HIRI. In this review, we summarized the latest research on lncRNAs, miRNAs and the lncRNA-miRNA regulatory networks in HIRI. DATA SOURCES: The PubMed and Web of Science databases were searched for articles published up to December 2021 using the following keywords: "hepatic ischemia-reperfusion injury", "lncRNA", "long non-coding RNA", "miRNA" and "microRNA". The bibliography of the selected articles was manually screened to identify additional studies. RESULTS: The mechanism of HIRI is complex, and involves multiple lncRNAs and miRNAs. The roles of lncRNAs such as AK139328, CCAT1, MALAT1, TUG1 and NEAT1 have been established in HIRI. In addition, numerous miRNAs are associated with apoptosis, autophagy, oxidative stress and cellular inflammation that accompany HIRI pathogenesis. Based on the literature, we conclude that four lncRNA-miRNA regulatory networks mediate the pathological progression of HIRI. Furthermore, the expression levels of some lncRNAs and miRNAs undergo significant changes during the progression of HIRI, and thus are potential prognostic markers and therapeutic targets. CONCLUSIONS: Complex lncRNA-miRNA-mRNA networks regulate HIRI progression through mutual activation and antagonism. It is necessary to screen for more HIRI-associated lncRNAs and miRNAs in order to identify novel therapeutic targets.

LncRNA XIST Promotes Migration and Invasion of Papillary Thyroid Cancer Cell by Modulating MiR-101-3p/CLDN1 Axis.

Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy in the worlds. Long non-coding RNA X-inactive specific transcript (XIST) was found to upregulate in PTC tissues and cell lines. However, the molecular mechanism underlying PTC metastasis and whether XIST plays regulatory role in PTC are still largely unknown. qRT-PCR was performed to detect the expression of lncRNA XIST and mRNAs. Western blotting was carried out to detect CLDN1, MMP2, and MMP9. Transwell assay was used to detect migration and invasion. Starbase bioinformatics prediction and luciferase assay were used to validate the relationship of miR-101-3p and XIST or CLDN1. LncRNA XIST was upregulated in PTC tissues and cells. XIST knockdown suppressed migration and invasion of PTC cells. XIST could directly bind with miR-101-3p. Overexpression of miR-101-3p suppressed migration and invasion of PTC cells. CLDN1 was the target of miR-101-3p, and overexpression of CLDN1 can reverse the inhibition of cell migration and invasion by miR-101-3p, What's more, miR-101-3p inhibition and CLDN1 overexpression can reverse the affection of sh-XIST on migration and invasion of PTC cells inhibition. XIST promotes migration and invasion of papillary thyroid cancer cell via directly regulating miR-101-3p/CLDN1 axis, which is a novel mechanistic of XIST in the regulation of PTC.

LINC00689 participates in proliferation, chemoresistance and metastasis via miR-31-5p/YAP/ß-catenin axis in colorectal cancer.

As a kind of high-incidence malignant tumors in the digestive tract, colorectal cancer (CRC) has extremely morbidity and mortality in the population. LncRNAs have been proved to regulate the proliferation, chemoresistance and metastasis of tumors including CRC. LINC00689 and miR-31-5p in CRC were found misregulated in CRC by TCGA analysis. However, the mechanism of LINC00689 and miR-31-5p in regulating CRC remains unknown. The expression levels of LINC00689, miR-31-5p and LATS2 in CRC tissues and cell lines were examined by qRT-PCR assay. Cell proliferation, metastasis (including invasion and migration) were quantified by MTT assay, colony formation and Transwell assay, respectively. Western blotting assay was then performed to verify the levels of YAP/ß-catenin and metastasis-related proteins. Dual-luciferase reporter assay and RIP assay were performed to evaluate the interaction between LINC00689 (LATS2) and miR-31-5p. Moreover, the function of LINC00689 and miR-31-5p were confirmed by CRC xenograft in nude mice. LINC00689 was decreased while miR-31-5p was increased in CRC. The overexpression of LINC00689 or the knockdown of miR-31-5p inhibited cell proliferation, chemoresistance and metastasis of CRC cells. Meanwhile, the up-regulated LATS2 suppressed the activity of YAP/ß-catenin pathway to repress CRC occurrence. Silencing LATS2 reversed the inhibition effects of overexpression of LINC00689 or knockdown of miR-31-5p on proliferation, chemoresistance and metastasis of CRC cells. LINC00689 indeed acted as a miR-31-5p sponge to inhibit CRC proliferation, chemoresistance and metastasis through up-regulating LATS2 and repressing YAP/ß-catenin signaling pathway.

Chemical composition and antimicrobial activity of the essential oils from Chloranthus japonicus Sieb. and Chloranthus multistachys Pei.

We examined the composition and antimicrobial activity of two essential oils from Chloranthus japonicus Sieb. and Chloranthus multistachys Pei. GC-FID and GC-MS analyses identified 48 and 39 compounds, which represented 95.56% and 94.58%, respectively, of all components in these oils. Of these, 28 compounds were common to both, with a relatively high amount of oxygenated monoterpenes (50.95% and 39.97%). Antimicrobial properties were evaluated in vitro via disc diffusion and microbroth dilution assays. Activities were strong against most tested microorganisms, with inhibition zones ranging from 8.1 to 22.2 mm. For both species, minimum values for inhibitory and bactericidal concentrations were 0.39 to 12.50 mg/mL and 0.78 to 50.00 mg/mL, respectively. These results suggest that these essential oils are potent natural sources of antimicrobial agents for the medicinal and pharmaceutical industries.