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Search Results (21)
  • Open Access

    ARTICLE

    3-epi-bufotalin suppresses the proliferation in colorectal cancer cells through the inhibition of the JAK1/STAT3 signaling pathway

    SANHUA LI1,2,#, QINGHONG KONG1,2,#, XIAOKE ZHANG1,2, XINTING ZHU1,3, CHUNBO YU3, CHANGYAN YU1,2, NIAN JIANG1,2, JING HUI1,2, LINGJIE MENG1,2,*, YUN LIU1,2,3,*

    BIOCELL, Vol.46, No.11, pp. 2425-2432, 2022, DOI:10.32604/biocell.2022.019916

    Abstract Traditional Chinese medicine (TCM) has been increasingly employed in the last decades in China for both preventing and treating a variety of cancers. 3-epi-bufotalin is an active ingredient of TCM “Chanpi” with anti-tumor potential. However, the effect and mechanism of 3-epi-bufotalin on colorectal cancers were not well disclosed. The present study demonstrated that 3-epi-bufotalin could reduce viability, trigger apoptosis, and block the cell cycle at the G2/M stage in colorectal cancer cell lines HT29, RKO, and COLO205 in vitro. Moreover, 3-epi-bufotalin inhibited the JAK1/STAT3 signaling pathway. These results indicated the anti-proliferation ability of 3-epi-bufotalin in colorectal cancer cells. More >

  • Open Access

    ARTICLE

    miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis

    Xue-Yi Yang, Ye Sheng

    Oncology Research, Vol.27, No.9, pp. 997-1006, 2019, DOI:10.3727/096504018X15439207752093

    Abstract Although miR-101 is involved in the development and progression of T-cell acute lymphoblastic leukemia (T-ALL), the underlying molecular mechanisms remain unclear. In this article, we report that miR-101 expression was inversely correlated with CX chemokine receptor 7 (CXCR7) level in T-ALL. Introducing miR-101 inhibited T-ALL cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis in vivo. CXCR7 was identified as a direct target of miR-101. The inhibitory effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. Mechanistically, miR-101 targets CXCR7/STAT3 axis to reduce T-ALL growth and metastasis. Overall, these findings implied the… More >

  • Open Access

    ARTICLE

    MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3

    Dan Shan, Yumin Shang, Tongxiu Hu

    Oncology Research, Vol.27, No.3, pp. 349-358, 2019, DOI:10.3727/096504018X15247361080118

    Abstract Cervical cancer is the third most common gynecological cancer and the fourth leading cause of cancer-related deaths in women around the world. Substantial evidence has demonstrated that microRNA (miRNA) expression is disordered in many malignant tumors. The dysregulation of miRNAs has been suggested to be involved in the tumorigenesis and tumor development of cervical cancer. Therefore, identification of miRNAs and their biological roles and targets involved in tumor pathology would provide valuable insight into the diagnosis and treatment of patients with cervical cancer. MicroRNA-411 (miR-411) has been reported to play an important role in several types of human cancer. However,… More >

  • Open Access

    ARTICLE

    TRIM14 Promotes Breast Cancer Cell Proliferation by Inhibiting Apoptosis

    Gaowu Hu, Wei Pen, Ming Wang

    Oncology Research, Vol.27, No.4, pp. 439-447, 2019, DOI:10.3727/096504018X15214994641786

    Abstract Tripartite motif-containing 14 (TRIM14) is abnormally expressed in several human cancers. However, the function and expression of TRIM14 in human breast cancer are still largely unknown. To understand the biological function of TRIM14 in breast cancer, we measured the expression level of TRIM14. Cell proliferation and cell apoptosis were measured after TRIM14 overexpression or knockdown. Upregulation of TRIM14 was found in human breast cancer specimens and cell lines. Reduction of TRIM14 inhibited cell proliferation but increased cell apoptosis in the BT474 and MDA-MB-231 cell lines. Further study showed that knockdown of TRIM14 upregulated the expression of BAX while downregulating the… More >

  • Open Access

    ARTICLE

    STAT3 Polymorphism Associates With mTOR Inhibitor-Induced Interstitial Lung Disease in Patients With Renal Cell Carcinoma

    Kazuhiro Yamamoto*, Takeshi Ioroi*, Kazuaki Shinomiya, Ayaka Yoshida*, Kenichi Harada, Masato Fujisawa, Tomohiro Omura*, Yasuaki Ikemi§, Shunsaku Nakagawa§, Atsushi Yonezawa§, Osamu Ogawa, Kazuo Matsubara§, Takuya Iwamoto#, Kohei Nishikawa**, Sayaka Hayashi††, Daichi Tohara††, Yoji Murakami‡‡, Takanobu Motoshima‡‡, Hirofumi Jono††, Ikuko Yano

    Oncology Research, Vol.29, No.1, pp. 11-23, 2021, DOI:10.3727/096504022X16418911579334

    Abstract We evaluated the association of signal transducer and activator of transcription 3 (STAT3) polymorphisms with the incidence of mammalian target of rapamycin (mTOR) inhibitor-induced interstitial lung disease (ILD) in patients with renal cell carcinoma (RCC). We also used lung-derived cell lines to investigate the mechanisms of this association. Japanese patients with metastatic RCC who were treated with mTOR inhibitors were genotyped for the STAT3 polymorphism, rs4796793 (−1697C/G). We evaluated the association of the STAT3 genotype with the incidence of ILD and therapeutic outcome. In the 57 patients included in the primary analysis, the ILD rate within 140 days was significantly… More >

  • Open Access

    ARTICLE

    BET protein inhibitor apabetalone represses Porphyromonas gingivalis LPS-induced macrophage M1 polarization via regulating miR-130a/STAT3 axis

    MEIHUA CHEN1,2, HUIHUI WANG3, XIAOFENG CHEN1,2, YAN CHEN1,2, TIANYING BIAN1,2,*

    BIOCELL, Vol.46, No.10, pp. 2281-2289, 2022, DOI:10.32604/biocell.2022.020697

    Abstract Periodontitis is a frequent chronic inflammatory disorder destroying periodontium. Recent studies have revealed the role of bromodomain and extraterminal domain inhibitor (BETi) and microRNA (miR)-130a in regulating macrophage polarization and pro-inflammatory response. However, little is known about whether apabetalone (a novel BETi) and miR-130a are correlated with chronic inflammatory state in periodontitis by regulating macrophage polarization. Here murine RAW264.7 macrophages were applied as an in vitro inflammatory model. After treatment with Porphyromonas gingivalis-derived lipopolysaccharide (Pg LPS) and apabetalone, the expression of macrophage M1 polarization markers and inflammatory cytokines was assessed using real-time PCR, western blot, and enzyme-linked immuno sorbent assay… More >

  • Open Access

    ARTICLE

    miRNA-148b-3p targeting SOCS3 inhibits macrophage M2 polarization by JAK2/STAT3 pathway in immune thrombocytopenia

    YANG YANG, LIJUAN FU, CHUNMEI CHEN, MEIWEI HU

    BIOCELL, Vol.46, No.5, pp. 1319-1328, 2022, DOI:10.32604/biocell.2022.015760

    Abstract Aberrant expression of miRNAs is significantly correlated with the occurrence of immune thrombocytopenic purpura (ITP). The immune imbalance of M1/M2 macrophage contributes to the development of ITP. However, the role of miR-148b-3p in macrophage phenotype imbalance remains unknown in ITP. In this study, we aimed to explore whether miR-148b-3p inhibits M2 macrophage polarization in ITP and to investigate the underlying mechanism. Peripheral blood from 22 ITP patients were collected, and real-time PCR confirmed that miR-148b-3p was up-regulated and Western blot analyses detected the expression of SOCS3 was down-regulated. Subsequent dual-luciferase reporter gene assay indicated that miR-148b-3p could bind to SOCS3.… More >

  • Open Access

    ARTICLE

    KIAA1199 induces advanced biological behavior and development of ovarian cancer through activation of the IL-6/STAT3 pathway

    SHUTING GU1,2,#, JINGYI QIN3,#, SAINAN GAO1, ZHEN WANG1,4, QI MENG1,4, YAN LI1,4, BING LU5, SONGLIN ZHOU1,2,*, YUNZHAO XU1,6,*

    BIOCELL, Vol.46, No.3, pp. 689-697, 2022, DOI:10.32604/biocell.2022.016225

    Abstract Recently, abnormal expression of KIAA1199 has been detected in Epithelial Ovarian Cancer (EOC). However, the underlined anti-ovarian cancer mechanism of KIAA1199 remains to be enlightened. In our study, we performed to elucidate the effects of KIAA1199 on the advanced biological behavior of EOC cells through activation of the IL-6/STAT3 pathway. Confirmed by immunohistochemistry, KIAA1199 was highly expressed in ovarian borderline and malignant epithelial tumors. A retrospective analysis found that EOC patients with low expression of KIAA1199 had a significantly higher 5-year survival rate than those with high expression. Mechanistically, IL-6 was used to stimulate EOC cells, and the expression of… More >

  • Open Access

    ARTICLE

    Protective effects of docosahexaenoic acid against non-alcoholic hepatic steatosis through activating of JAK2/STAT3 signaling pathway

    YUE WANG1,#, YINPING DUAN1,#, KUNLIN CHEN3, HUIXIA LI1,2,*, YAN QUAN4,*

    BIOCELL, Vol.45, No.2, pp. 307-316, 2021, DOI:10.32604/biocell.2021.014305

    Abstract Non-alcoholic fatty liver disease is the most common cause of hepatic dysfunction. In the present study, human normal hepatocyte L02 cells were treated with 50% fetal bovine serum to induce the formation of hepatic steatosis in vitro, and then the cells were treated with docosahexaenoic acid to investigate its protective effect on Non-alcoholic fatty liver disease. Our results showed that 50% of fetal bovine serum significantly induced intracellular lipid accumulation and hepatocyte fatty degeneration within 48 h. The expression level of adipose formation-related genes was significantly up-regulated, such as PPARγ, C/EBPα and SREBP-1; meanwhile, the content of cellular total lipid,… More >

  • Open Access

    ARTICLE

    Spontaneous running wheel improves neuroprotection efficacy of ischemic postconditioning in mice following ischemia/reperfusion injury

    Hong YE1,6,#, WeiWei Wang2,#, Yu Ding3,#, XiaoLei Liu4,#, WenJI Jia1, WeiLi Luo1, HuiJuan Fan1, HongQun Zhou1, Jin Wang1, JianLong Ju1, DongMing Zhou7, TianHao Bao5,1,*, YuHong Zhu1,*

    BIOCELL, Vol.42, No.3, pp. 79-86, 2018, DOI:10.32604/biocell.2018.04615

    Abstract Ischemic postconditioning (IP) has been shown to provide protection for ischemia/reperfusion (IR) injury, but its efficacy is limited. In this study we hypothesized that spontaneous running wheel (RW) could improve neuroprotection efficacy of IP for IR. We established mouse models of IR and showed that compared to Sham group, IR group had obvious brain infract and neurological dysfunction. In IR+IP group, brain infract and neurological dysfunction improved compared to IR group. However, in IR+IP+RW group brain infract and neurological dysfunction improved much better. TUNEL assay showed that IP but not RW significantly reduced the number of apoptotic cells after IR.… More >

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