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  1. Article ; Online: RNA Interference Approach Is a Good Strategy against SARS-CoV-2.

    Lee, Ying-Ray / Tsai, Huey-Pin / Yeh, Chun-Sheng / Fang, Chiung-Yao / Chan, Michael W Y / Wu, Tzu-Yun / Shen, Cheng-Huang

    Viruses

    2022  Volume 15, Issue 1

    Abstract: COVID-19, caused by SARS-CoV-2, created a devastating outbreak worldwide and consequently became a global health concern. However, no verifiable, specifically targeted treatment has been devised for COVID-19. Several emerging vaccines have been used, but ...

    Abstract COVID-19, caused by SARS-CoV-2, created a devastating outbreak worldwide and consequently became a global health concern. However, no verifiable, specifically targeted treatment has been devised for COVID-19. Several emerging vaccines have been used, but protection has not been satisfactory. The complex genetic composition and high mutation frequency of SARS-CoV-2 have caused an uncertain vaccine response. Small interfering RNA (siRNA)-based therapy is an efficient strategy to control various infectious diseases employing post-transcriptional gene silencing through the silencing of target complementary mRNA. Here, we designed two highly effective shRNAs targeting the conserved region of RNA-dependent RNA polymerase (RdRP) and spike proteins capable of significant SARS-CoV-2 replication suppression. The efficacy of this approach suggested that the rapid development of an shRNA-based therapeutic strategy might prove to be highly effective in treating COVID-19. However, it needs further clinical trials.
    MeSH term(s) Humans ; COVID-19/therapy ; RNA Interference ; RNA, Small Interfering/genetics ; RNA-Dependent RNA Polymerase/genetics ; RNA-Dependent RNA Polymerase/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism
    Chemical Substances RNA, Small Interfering ; RNA-Dependent RNA Polymerase (EC 2.7.7.48)
    Language English
    Publishing date 2022-12-29
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v15010100
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Ivermectin induces cell cycle arrest and caspase-dependent apoptosis in human urothelial carcinoma cells.

    Tung, Chun-Liang / Chao, Wen-Ying / Li, Yi-Zhen / Shen, Cheng-Huang / Zhao, Pei-Wen / Chen, Shu-Hsin / Wu, Tzu-Yun / Lee, Ying-Ray

    International journal of medical sciences

    2022  Volume 19, Issue 10, Page(s) 1567–1575

    Abstract: Bladder carcinoma is one of the most common malignancies worldwide, and >90% of all bladder cancers are classified as urothelial carcinomas (UC). Surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy are evidence-based treatments that ... ...

    Abstract Bladder carcinoma is one of the most common malignancies worldwide, and >90% of all bladder cancers are classified as urothelial carcinomas (UC). Surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy are evidence-based treatments that are administered depending on the clinical stage of UC. All these treatments exhibited limited effects in cases of metastatic UC, and UC with specific location, invasiveness, and recurrence. Therefore, a new therapeutic strategy for UC is urgently needed. Ivermectin, an avermectin derivative, has been reported to be effective against various parasites, and its pharmacokinetic and pharmacodynamic properties as well as safety are well understood in humans. Recently, ivermectin was shown to exhibit therapeutic benefits against various virus infections
    MeSH term(s) Apoptosis ; Carcinoma, Transitional Cell ; Caspases ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Ivermectin/pharmacology ; Ivermectin/therapeutic use ; JNK Mitogen-Activated Protein Kinases ; Urinary Bladder Neoplasms/pathology
    Chemical Substances Ivermectin (70288-86-7) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2022-09-11
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2151424-0
    ISSN 1449-1907 ; 1449-1907
    ISSN (online) 1449-1907
    ISSN 1449-1907
    DOI 10.7150/ijms.76623
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Bufalin induces cell death in human lung cancer cells through disruption of DNA damage response pathways.

    Wu, Shin-Hwar / Wu, Tzu-Yun / Hsiao, Yung-Ting / Lin, Ju-Hwa / Hsu, Shu-Chun / Hsia, Te-Chun / Yang, Su-Tso / Hsu, Wu-Huei / Chung, Jing-Gung

    The American journal of Chinese medicine

    2014  Volume 42, Issue 3, Page(s) 729–742

    Abstract: Bufalin is a key component of a Chinese medicine (Chan Su) and has been proved effective in killing various cancer cells. Its role in inducing DNA damage and the inhibition of the DNA damage response (DDR) has been reported, but none have studied such ... ...

    Abstract Bufalin is a key component of a Chinese medicine (Chan Su) and has been proved effective in killing various cancer cells. Its role in inducing DNA damage and the inhibition of the DNA damage response (DDR) has been reported, but none have studied such action in lung cancer in detail. In this study, we demonstrated bufalin-induced DNA damage and condensation in NCI-H460 cells through a comet assay and DAPI staining, respectively. Western blotting indicated that bufalin suppressed the protein levels associated with DNA damage and repair, such as a DNA dependent serine/threonine protein kinase (DNA-PK), DNA repair proteins breast cancer 1, early onset (BRCA1), 14-3-3 σ (an important checkpoint keeper of DDR), mediator of DNA damage checkpoint 1 (MDC1), O6-methylguanine-DNA methyltransferase (MGMT) and p53 (tumor suppressor protein). Bufalin could activate phosphorylated p53 in NCI-H460 cells. DNA damage in NCI-H460 cells after treatment with bufalin up-regulated its ATM and ATR genes, which encode proteins functioning as sensors in DDR, and also up-regulated the gene expression (mRNA) of BRCA1 and DNA-PK. But bufalin suppressed the gene expression (mRNA) of p53 and 14-3-3 σ, however, bufalin did not significantly affect the mRNA of MGMT. In conclusion, bufalin induced DNA damage in NCI-H460 cells and also inhibited its DNA repair and checkpoint function.
    MeSH term(s) 14-3-3 Proteins/metabolism ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Apoptosis/genetics ; BRCA1 Protein/metabolism ; Biomarkers, Tumor/metabolism ; Bufanolides/pharmacology ; DNA Damage/drug effects ; DNA Damage/genetics ; DNA Modification Methylases/metabolism ; DNA Repair/drug effects ; DNA Repair/genetics ; DNA Repair Enzymes/metabolism ; DNA-Activated Protein Kinase/metabolism ; Exoribonucleases/metabolism ; Genes, cdc/drug effects ; Genes, cdc/genetics ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Nuclear Proteins/metabolism ; Trans-Activators/metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/metabolism
    Chemical Substances 14-3-3 Proteins ; Antineoplastic Agents ; BRCA1 Protein ; BRCA1 protein, human ; Biomarkers, Tumor ; Bufanolides ; MDC1 protein, human ; Nuclear Proteins ; Trans-Activators ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins ; chan su ; DNA Modification Methylases (EC 2.1.1.-) ; MGMT protein, human (EC 2.1.1.63) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; Exoribonucleases (EC 3.1.-) ; SFN protein, human (EC 3.1.-) ; DNA Repair Enzymes (EC 6.5.1.-) ; bufalin (U549S98QLW)
    Language English
    Publishing date 2014
    Publishing country Singapore
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 193085-0
    ISSN 0192-415X ; 0090-2942
    ISSN 0192-415X ; 0090-2942
    DOI 10.1142/S0192415X14500475
    Database MEDical Literature Analysis and Retrieval System OnLINE

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