Publications by authors named "Jinhui Guo"

8 Publications

  • Page 1 of 1

HIF-1α-activated TM4SF1-AS1 promotes the proliferation, migration, and invasion of hepatocellular carcinoma cells by enhancing TM4SF1 expression.

Biochem Biophys Res Commun 2021 Aug 10;566:80-86. Epub 2021 Jun 10.

The Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, 310014, China. Electronic address:

Long non-coding RNAs (lncRNAs) are essential drivers or suppressors in human hepatocellular carcinoma (HCC) by participating in controlling transcription, translation, mRNA stability, and protein degradation protein-protein interaction. TM4SF1-AS1 is recently identified as a tumor-promoting factor in lung cancer. Nevertheless, its function in HCC and related molecular mechanisms remain unknown. Here, our data indicated that either hypoxia or hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor (DMOG) induced the upregulation of TM4SF1-AS1 in HCC cells. HIF-1α knockdown rather than HIF-2α silencing remarkably abrogated hypoxia-upregulated TM4SF1-AS1 expression. Furthermore, we confirmed the elevated expression of TM4SF1-AS1 in HCC tissue samples and cell lines. The silencing of TM4SF1-AS1 prominently inhibited the proliferative, migratory, and invasive abilities of HCC cells. TM4SF1-AS1 depletion significantly blocked hypoxia-enhanced Hep3B cell proliferation and mobility. Interfering TM4SF1-AS1 remarkably reduced TM4SF1 mRNA and protein levels in HCC cells. But TM4SF1-AS1 knockdown did not impact the stability of TM4SF1 mRNA. Hypoxia enhanced the expression of TM4SF1 mRNA, which was subsequently decreased by TM4SF1-AS1 knockdown in HCC cells. We confirmed the positive correlation between TM4SF1 mRNA and TM4SF1-AS1 expression in HCC specimens. Finally, TM4SF1 prominently reversed the inhibitory role of TM4SF1-AS1 depletion in Hep3B cells. In summary, hypoxia-responsive TM4SF1-AS1 was overexpressed in human HCC and contributed to the malignant behaviors of tumor cells by enhancing TM4SF1-AS1 expression.
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http://dx.doi.org/10.1016/j.bbrc.2021.06.011DOI Listing
August 2021

Effects of resveratrol in the signaling of neuropathic pain involving P2X3 in the dorsal root ganglion of rats.

Acta Neurol Belg 2021 Apr 15;121(2):365-372. Epub 2019 Apr 15.

Department of Pharmaceutics, the First Affiliated Hospital of Xinxiang Medical University, No. 88 Jiankang Road, Weihui, 453100, Henan, People's Republic of China.

Neuropathic pain is a major public health problem because it has a considerable impact on life quality of patients. Neuropathic pain caused by a lesion or disease of the somatosensory nervous system, which causes unpleasant and abnormal sensation (dysesthesia), an increased response to painful stimuli (hyperalgesia), and pain in response to a stimulus that does not normally provoke pain (allodynia). P2X receptors from dorsal root ganglion (DRG) play a crucial role in facilitating pain transmission at peripheral and spinal sites. Resveratrol (Res) has neuroprotective effects and improves the pathological and behavioral outcomes of various types of nerve injury. The present study examined the effects of Res on neuropathic pain. Neuropathic pain animal model was created by partial sciatic nerve ligation (pSNL) surgery. We found that consecutive intraperitoneal administration of Res for 21 days reduced the mechanical and thermal nociceptive responses induced by pSNL in a dose-dependent manner. Moreover, Res administration reversed P2X3 expression and phosphorylation of ERK in DRG neurons after peripheral nerve injury. Our results suggested that Res may ameliorate neuropathic pain by suppressing P2X3 up-regulation and ERK phosphorylation in DRG of neuropathic pain rats. Therefore, we concluded that Res has a significant analgesic effect on alleviating neuropathic pain, and thus may serve as a therapeutic approach for neuropathic pain.
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http://dx.doi.org/10.1007/s13760-019-01126-2DOI Listing
April 2021

Euxanthone suppresses tumor growth and metastasis in colorectal cancer via targeting CIP2A/PP2A pathway.

Life Sci 2018 Sep 23;209:498-506. Epub 2018 Aug 23.

People's Hospital of Henan, Henan, China.

Aim: Colorectal cancer (CRC) accounts for over 600,000 deaths annually worldwide. Euxanthone is a flavonoid compound extracted from Polygala caudata, with documented anti-neoplastic actions. The current study aimed to determine the therapeutic potential of euxanthone in CRC.

Methods And Materials: Cell Counting Kit-8 (CCK-8) assay was used to analyze the effect of euxanthone on the cell viability, and apoptosis was detected by the TUNEL assay. The in vitro migratory capacity was determined by wound healing and the invasiveness was assessed by Transwell assay. Western blotting was used to determine the level of relevant proteins. Furthermore, a CRC xenograft murine model was used to analyze the therapeutic efficacy of euxanthone in vivo. Isobaric tags for relative and absolute quantification (iTRAQ) was then performed to identify the potential targets of euxanthone. To validate the role of cancerous inhibitor of PP2A (CIP2A) in the anti-cancer effects of euxanthone, plasmid overexpressing CIP2A and shRNA targeting CIP2A were used in in vitro assays.

Key Findings: Euxanthone decreased cell viability and increased apoptosis in CRC cells, in addition to restraining migration, invasion and EMT. Similarly, euxanthone also effectively suppressed tumor growth and pulmonary metastasis in vivo. iTRAQ analysis identified CIP2A as the primary target responsible for the anticancer effects of euxanthone. The mediatory role of CIP2A was validated when the anticancer activity of euxanthone was significantly blocked by CIP2A overexpression, while CIP2A knockdown sensitized the CRC cells to euxanthone.

Significance: Euxanthone exerts anti-cancer effects in vitro and in vivo in CRC by targeting CIP2A/PP2A signaling.
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http://dx.doi.org/10.1016/j.lfs.2018.08.052DOI Listing
September 2018

Long noncoding RNA eosinophil granule ontogeny transcript inhibits cell proliferation and migration and promotes cell apoptosis in human glioma.

Exp Ther Med 2017 Oct 16;14(4):3817-3823. Epub 2017 Aug 16.

Department of Oncology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China.

Glioma is the most common primary brain tumor and represents one of the most aggressive and lethal types of human cancer. Recent advances have implicated long noncoding RNAs (lncRNAs) as crucial mediators of cancer development and progression. The present study aimed to investigate the role of a newly-discovered lncRNA, termed eosinophil granule ontogeny transcript (EGOT), in the aggressive abilities of cells in human glioma. It was initially found that the relative transcription level of EGOT in glioma cancerous tissues was significantly lower than that in adjacent non-cancerous tissues. EGOT was differentially expressed in a series of glioma cell lines, with its lowest level in high aggressive U251 and U87 cells. When EGOT was overexpressed by an expression plasmid, cell viability was significantly inhibited in U251 and U87 cells. Furthermore, with EGOT overexpression, the cell cycle was arrested at G0/G1 phase and consequently, cell apoptosis was significantly promoted along with the activities of caspase-3 and caspase-9. The migration abilities of EGOT-overexpressed cells were inhibited by 71.4% in U251 cells and by 69.5% in U87 cells. These data suggest that overexpression of EGOT inhibits cell proliferation and migration, and promotes cell apoptosis in glioma. Therefore, EGOT has potent anticancer activity and may function as a tumor suppressor in human glioma.
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http://dx.doi.org/10.3892/etm.2017.4949DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5639339PMC
October 2017

Super-compact treatment with a high dose of moxifloxacin in patients with drug-resistant tuberculosis and its resistance mechanisms.

Exp Ther Med 2015 Apr 29;9(4):1314-1318. Epub 2015 Jan 29.

Department of Tuberculosis, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China.

The aim of this study was to investigate the curative effect and resistance mechanisms of high-dose moxifloxacin in the short-term treatment of multidrug-resistant tuberculosis. A total of 92 patients with multidrug-resistant tuberculosis were randomly selected and divided into groups A and B (n=46 per group). The two groups received moxifloxacin treatment with the same dose in total. Group A received a short course of treatment with moxifloxacin (0.6 g/day for 6 months), whereas group B received normal moxifloxacin treatment (0.4 g/day for 9 months). Sputum negative conversion, foci absorption, cavity closure and adverse reactions in the two groups were observed, and the drug resistance mechanism of tuberculosis to moxifloxacin treatment was investigated. Following the treatment, the curative rate of group A was 82.61%, and the curative rate of group B was 84.78%; there was no statistically significant difference between the two groups (P>0.05). The rates of sputum negative conversion, foci absorption and cavity closure were not significantly different between the two groups (P>0.05). However, the rates of reduction in peripheral white blood cell counts, liver function damage and adverse reactions, including symptoms affecting the gastrointestinal and nervous systems, were significantly lower in group A than in group B (P<0.05). The expression levels of the antigen-presenting functional molecules CD80 and CD40 on the surfaces of mononuclear cells were higher in group A than in group B (P<0.05), whereas the difference in HLA-DR expression between groups A and B was not significant (P>0.05). In conclusion, short-term treatment with a high dose of moxifloxacin is effective for multidrug-resistant tuberculosis, and its advantages are a reduction in the incidence of drug-associated adverse reactions and a lack of drug resistance.
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http://dx.doi.org/10.3892/etm.2015.2230DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4353789PMC
April 2015

Significant reduction of antibiotic consumption and patients' costs after an action plan in China, 2010-2014.

PLoS One 2015 13;10(3):e0118868. Epub 2015 Mar 13.

Department of Pharmacy, Central Hospital, Xinyang, Henan, China.

Introduction: On July 1, 2011, the Chinese government launched a national Action Plan for antibiotic stewardship targeting antibiotic misuse in public hospitals. The aim of this study was to evaluate the impacts of the Action Plan in terms of frequency and intensity of antibiotic utilization and patients costs in public general hospitals.

Methods: Administrative pharmacy data from July 2010 to June 2014 were sampled from 65 public general hospitals and divided into three segments: (1) July 2010 to June 2011 as the preparation period; (2) July 2011 to June 2012 as the intervention period; and (3) July 2012 to June 2014 as the assessment period. The outcome measures included (1) antibiotic prescribing rates; (2) intensity of antibiotic consumption; (3) patients costs; and (4) duration of peri-operative antibiotic treatment in clean surgeries of thyroidectomy, breast, hernia, and orthopedic procedures. Longitudinal and cross-sectional analyses were conducted.

Results: Longitudinal analyses showed significant trend changes in the frequency and intensity of antibiotic consumption, the patients' costs on antibiotics, and the duration of antibiotic treatment received by surgical patients undergoing the 4 clean procedures during the intervention period. Cross-sectional analyses showed that the antibiotic prescribing rates were reduced to 35.3% and 12.9% in inpatient and outpatient settings, that the intensity of antibiotic consumption was reduced to 35.9 DDD/100 bed-days, that patients' costs on antibiotics were reduced significantly, and that the duration of peri-operative antibiotic treatment received by surgical patients undergoing the 4 types of clean procedures decreased to less than 24 hour during the assessment period.

Conclusion: The Action Plan, as a combination of managerial and professional strategies, was effective in reducing the frequency and intensity of antibiotic consumption, patients' costs on antibiotics, and the duration of peri-operative antibiotic treatment in the 4 clean surgeries.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0118868PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4359138PMC
January 2016

Ginsenoside compound K promotes β-amyloid peptide clearance in primary astrocytes via autophagy enhancement.

Exp Ther Med 2014 Oct 6;8(4):1271-1274. Epub 2014 Aug 6.

Department of Pharmaceutics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China.

The aim of the present study was to investigate the effect of ginsenoside compound K on β-amyloid (Aβ) peptide clearance in primary astrocytes. Aβ degradation in primary astrocytes was determined using an intracellular Aβ clearance assay. Aggregated LC3 in astrocyte cells, which is a marker for the level of autophagy, was detected using laser scanning confocal microscope. The effect of compound K on the mammalian target of rapamycin (mTOR)/autophagy pathway was determined using western blot analysis, and an enzyme-linked immunosorbent assay was used for Aβ detection. The results demonstrated that compound K promoted the clearance of Aβ and enhanced autophagy in primary astrocytes. In addition, it was found that phosphorylation of mTOR was inhibited by compound K, which may have contributed to the enhanced autophagy. In conclusion, compound K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.
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http://dx.doi.org/10.3892/etm.2014.1885DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151796PMC
October 2014

Mechanism underlying hypokalemia induced by trimethyltin chloride: Inhibition of H+/K+-ATPase in renal intercalated cells.

Toxicology 2010 Apr 6;271(1-2):45-50. Epub 2010 Mar 6.

Guangdong Poison Control Center, 68 Haikang St. Xingangxi Rd., Guangzhou, 510300, China.

Trimethyltin chloride (TMT), a byproduct of plastic stabilizers, has caused 67 poisoning accidents in the world; more than 98% (1814/1849) of the affected patients since 1998 have been in China. As a long-established toxic chemical, TMT severely affects the limbic system and the cerebellum; however, its relationship with hypokalemia, a condition observed in the majority of the cases in the last decade, remains elusive. To understand the mechanism underlying hypokalemia induced by TMT, Sprague-Dawley (SD) rats were administered TMT to determine the relationship between H(+)/K(+)-ATPase activity and the blood and urine K(+) concentration and pH, respectively. H(+)/K(+)-ATPase protein and mRNA were observed too. In vitro changes to intracellular pH, K(+) channels in renal cells were measured. The results showed that TMT increased potassium leakage from the kidney, raised urine pH, and inhibited H(+)/K(+)-ATPase activity both in vitro and in vivo. In the tested animals, H(+)/K(+)-ATPase activity was positively correlated with the decrease of plasma K(+) and blood pH but was negatively correlated with the increase of urine K(+) and urine pH (P<0.01), while TMT did not change the expression of H(+)/K(+)-ATPase protein and mRNA. TMT decreased intracellular pH and opened K(+) channels in renal intercalated cells. Our findings suggest TMT can directly inhibit the activity of H(+)/K(+)-ATPases in renal intercalated cells, reducing urine K(+) reabsorption and inducing hypokalemia.
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http://dx.doi.org/10.1016/j.tox.2010.02.013DOI Listing
April 2010
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