Publications by authors named "Lingling Miao"

Background: Index hopping causes read assignment errors in data from multiplexed sequencing libraries. This issue has become more prevalent with the widespread use of high-capacity sequencers and highly multiplexed single-cell RNA sequencing (scRNA- seq).

Results: We conducted deep, plate-based scRNA-seq on a mixed population of mouse skin cells.

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Background: According to the indexes of serum and anal function, acupuncture therapy was applied to patients with low rectal cancer in order to avoid the occurrence of anal incontinence and reduce complications.

Aim: To explore the clinical application and evaluate the effect of acupuncture therapy for anal function rehabilitation after low-tension rectal cancer surgery.

Methods: From the anorectal surgery cases, we selected 120 patients who underwent colorectal cancer surgery between January 2020 and December 2022 and randomly divided them into a control group ( = 60), observation group ( = 60), and control group after surgery for lifestyle intervention (including smoking cessation and exercise), dietary factor adjustment, anal movement, and oral loperamide treatment.

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Article Synopsis
  • Merkel cell carcinoma (MCC) and small cell lung cancer (SCLC) can look similar under a microscope, complicating their diagnosis and requiring specific tests to tell them apart.* -
  • Current immunohistochemistry markers like cytokeratin 20 (CK20) and thyroid transcription factor 1 (TTF-1) are commonly used, but have limitations in sensitivity and specificity.* -
  • New candidate markers, ATOH1 and TFAP2B for MCC, and CEACAM6 for SCLC, show high specificity and sensitivity in immunostaining, suggesting their potential in improving diagnostic accuracy.*
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Importance: Racial and ethnic differences in skin cancer outcomes are understudied. Delineating these differences in Merkel cell carcinoma (MCC) is needed to better understand this rare disease.

Objective: To determine how MCC presentation and outcomes differ across racial and ethnic groups.

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Background: Hepatocellular carcinoma (HCC) is characterised by high malignancy, metastasis and recurrence, but the specific mechanism that drives these outcomes is unclear. Recent studies have shown that long noncoding RNAs (lncRNAs) can regulate the proliferation and apoptosis of hepatic cells.

Methods: We searched for lncRNAs and microRNAs (miRNAs), which can regulate IGF1 expression, through a bioinformatics website, and predicted that lncRNA taurine-upregulated gene 1 (TUG1) would have multiple targets for miR-1-3p binding, meaning that lncRNA TUG1 played an adsorption role.

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MicroRNAs (miRNAs) are a class of endogenous small noncoding RNAs that participate in a majority of biological processes via regulating target gene expression. The post-transcriptional repression through miRNA seed region binding to 3' UTR of target mRNA is considered as the canonical mode of miRNA-mediated gene regulation. However, emerging evidence suggests that other regulatory modes exist beyond the canonical mechanism.

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Background: This study aimed to examine the switch from glargine+once daily insulin aspart (1 + 1 regimen) to glargine+insulin aspart 30 before breakfast combined with exercise and in patients with type 2 diabetes mellitus (T2DM) with poorly controlled blood glucose levels.

Methods: Consecutive patients with poorly controlled T2DM (n = 182) were switched from the 1 + 1 regimen to glargine+insulin aspart 30 before breakfast in combination with exercise after dinner and dividing meals in two (same final calories intake). The insulin doses were adjusted according to blood glucose levels within 4 weeks after the switch and maintained for 12 weeks.

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Merkel cell carcinoma (MCC) is a rare and aggressive skin cancer that responds to PD-1/PD-L1 immune checkpoint inhibitors. CD200 is another checkpoint modulator whose receptor is found on tumor-promoting myeloid cells, including M2 macrophages. We found high mRNA expression in MCC tumors, and CD200 immunostaining was demonstrated on 95.

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As one of main obstacles in the treatment and prognosis of hepatocellular carcinoma (HCC), multidrug resistance (MDR) is usually associated with the overexpression of the drug efflux pump P-glycoprotein (P-gp/ABCB1) which is responsible for reducing the intracellular concentration of chemotherapeutic agents. In current work, we discovered the novel role of miR-491-3p in ABCB1-mediated multidrug resistance in HCC and revealed the underlying mechanism in which miR-491-3p downregulated the expression of ABCB1 and its transcription factor Sp3 by directly targeting their 3'-UTR. Moreover, overexpressing ABCB1 or Sp3 reversed the sensitivity to chemotherapeutics in Hep3B cells induced by miR-491-3p, confirming miR-491-3p/Sp3/ABCB1 regulatory loop plays an important role in enhancing the drugs sensitivity of HCC.

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MicroRNAs (miRNAs) are a class of small non-coding RNAs, which direct post-transcriptional gene silencing (PTGS) and function in a vast range of biological events including cancer development. Most miRNAs pair to the target sites through seed region near the 5' end, leading to mRNA cleavage and/or translation repression. Here, we demonstrated a miRNA-induced dual regulation of heme oxygenase-1 (HO-1) via seed region and non-seed region, consequently inhibited tumor growth of NSCLC.

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1,2:5,6-dianhydrogalactitol (DAG) is a hexitol epoxide with marked antitumor activity against multiple types of cancer cells, but the molecular mechanisms by which DAG functions as an antitumor agent is largely unknown. In this study, we investigated the inhibitory effects of DAG on human glioma cell growth in vitro and in vivo and uncovered the underlying molecular mechanisms. Treatment with DAG (120 μmol/L) dose-dependently inhibited the proliferation and colony formation in human glioma cell lines LN229, U251, and U87MG in vitro.

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Dicer1 is an enzyme essential for microRNA (miRNA) maturation. The loss of miRNAs resulted from Dicer1 deficiency greatly contributes to the progression of many diseases, including lipid dysregulation, but its role in hepatic accumulation of free cholesterol (FC) that is critical in the development of non-alcoholic steatohepatitis (NASH) remains elusive. In this study, we used the liver-specific Dicer1-knockout mice to identify the miRNAs involved in hepatic FC accumulation.

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Previous studies have shown that microRNA-1304 (miR-1304) is dysregulated in certain types of cancers, including non-small cell lung cancer (NSCLC), and might be involved in tumor survival and/or growth. In this study we investigated the direct target of miR-1304 and its function in NSCLC in vitro. Human lung adenocarcinoma cell lines (A549 and NCI-H1975) were studied.

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Multidrug resistance-associated protein 1 (MRP1) is an important efflux transporter and overexpression of MRP1 usually leads to chemoresistance in breast cancer. Here, we found MRP1 overexpressed in human breast cancer tissues and breast cancer cell lines (compared with normal breast tissues and cell line, respectively). And MRP1 level increased in doxorubicin resistant MCF-7 cells compared with parental MCF-7 cells.

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The Sonic hedgehog (Shh) signaling pathway regulates developmental, homeostatic, and repair processes throughout the body. In the skin, touch domes develop in tandem with primary hair follicles and contain sensory Merkel cells. The developmental signaling requirements for touch dome specification are largely unknown.

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MicroRNAs (miRNAs) can direct post-transcriptional or transcriptional gene silencing. Here, we report that miR-552 is in the nucleus and cytosol and inhibits human cytochrome P450 (CYP) 2E1 expression at both transcriptional and post-transcriptional levels. MiR-552 via its non-seed sequence forms hybrids with a loop hairpin of the cruciform structure in CYP2E1 promoter region to inhibit SMARCE1 and RNA polymerase II binding to the promoter and CYP2E1 transcription.

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The aim of the present study was to examine the role of protease-activated receptor-1 (PAR1)-stimulated platelet activation in the epithelial-mesenchymal transition (EMT) and migration of colon cancer cells, and to identify the underlying mechanisms. TFLLR-NH2, a PAR1 agonist, was used to activate platelets and the platelet supernatants were used to treat the SW620 colon cancer cell line. Expression of E-cadherin and vimentin on SW620 cells was detected by immunofluorescence and western blotting, and the level of the transforming growth factor β1 (TGF-β1) was measured using ELISA following the activation of platelets by TFLLR-NH2.

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Aim: Tetrandrine, an alkaloid with a remarkable pharmacological profile, induces oxidative stress and mitochondrial dysfunction in hepatocytes; however, mitochondria are not the direct target of tetrandrine, which prompts us to elucidate the role of oxidative stress in tetrandrine-induced mitochondrial dysfunction and the sources of oxidative stress.

Methods: Rat primary hepatocytes were isolated by two-step collagenase perfusion. Mitochondrial function was evaluated by analyzing ATP content, mitochondrial membrane potential (MMP) and the mitochondrial permeability transition.

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Mouse cytochrome P450 2b9 (Cyp2b9) is a testosterone 16α-hydroxylase enzyme showing female-specific expression in many inbred mouse strains, including C57BL/6J. Previous studies have recognized that some sex-dependently secreted endogenous modulating factors were involved in the sexually dimorphic expression of Cyp2b9 through transcriptional regulation. In this study, we found evidence that some microRNAs contributed to the sexually biased expression of Cyp2b9 via post-transcriptional regulation.

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Genotoxicity assessment is of great significance in drug safety evaluation, and microarray is a useful tool widely used to identify genotoxic stress responsive genes. In the present work, by using oligonucleotide microarray in an in vivo model, we identified an unknown gene BC005512 (abbreviated as BC, official full name: cDNA sequence BC005512), whose expression in mouse liver was specifically induced by seven well-known genotoxins (GTXs), but not by non-genotoxins (NGTXs). Bioinformatics revealed that BC was a member of the GLN family of murine endogenous retrovirus (ERV).

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The central pore of a nuclear pore complex (NPC) is filled with unstructured proteins that contain many FG-repeats separated by hydrophilic regions. An example of such protein is nsp1. By simulating an array of nsp1 segments, we identified, in an earlier study, a spontaneously formed brushlike structure that promises to explain selective transport in the NPC channel.

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Nuclear pore complexes (NPCs) are selectively gated pathways between nucleoplasm and cytoplasm. Whereas small molecules can diffuse freely through NPCs, large molecules (>40 kD) can pass only when bound to transport receptors. The NPC central channel is filled with disordered proteins, rich in phenylalanine-glycine (FG) repeats, referred to as FG-nups.

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