• 제목/요약/키워드: proliferation, migration

검색결과 609건 처리시간 0.033초

Downregulated CDK10 promotes cancer progression and radioresistance in lung cancer through activating the JNK/c-Jun signaling pathway

  • Chaojin Hong;Yimei Meng;Anchen Qiu;Haibo Zhang;Liu Yang;Yupeng Hong;Yumei Huang
    • BMB Reports
    • /
    • 제57권7호
    • /
    • pp.336-341
    • /
    • 2024
  • Lung cancer is one of the most significant malignancies, with both high morbidity and mortality. CDK10 is closely related to cancer progression and metastasis. However, its role in lung cancer radioresistance demands further clarification. In this study, we demonstrated that CDK10 was downregulated in lung cancer tissues, and CDK10 expression level was associated with the clinical prognosis in lung cancer patients. We also found that silencing CDK10 promoted lung cancer cell proliferation, migration, and radioresistance. We further verified that silencing CDK10 facilitated the activation of JNK/c-Jun signaling, and c-Jun depletion could reverse the effects of CDK10 knockdown in lung cancer cells. Our findings revealed that CDK10 plays an important role in cell growth and radioresistance by inhibiting JNK/c-Jun signaling pathway in lung cancer. Therefore, CDK10 might be a promising therapeutic target in lung cancer.

Recombinant Human IL-32θ Induces Polarization Into M1-like Macrophage in Human Monocytic Cells

  • Hyo-Min Park;Jae-Young Park;Na-Yeon Kim;Hyemoon Kim;Hong-Gyum Kim;Dong-Ju Son;Jin Tae Hong;Do-Young Yoon
    • IMMUNE NETWORK
    • /
    • 제24권3호
    • /
    • pp.27.1-27.14
    • /
    • 2024
  • The tumor microenvironment (TME) is formed by several immune cells. Notably, tumor-associated macrophages (TAMs) are existed in the TME that induce angiogenesis, metastasis, and proliferation of cancer cells. Recently, a point-mutated variant of IL-32θ was discovered in breast cancer tissues, which suppressed migration and proliferation through intracellular pathways. Although the relationship between cancer and IL-32 has been previously studied, the effects of IL-32θ on TAMs remain elusive. Recombinant human IL-32θ (rhIL-32θ) was generated using an Escherichia coli expression system. To induce M0 macrophage polarization, THP-1 cells were stimulated with PMA. After PMA treatment, the cells were cultured with IL-4 and IL-13, or rhIL-32θ. The mRNA level of M1 macrophage markers (IL-1β, TNFα, inducible nitric oxide synthase) were increased by rhIL-32θ in M0 macrophages. On the other hand, the M2 macrophage markers (CCL17, CCL22, TGFβ, CD206) were decreased by rhIL-32θ in M2 macrophages. rhIL-32θ induced nuclear translocation of the NF-κB via regulation of the MAPK (p38) pathway. In conclusion, point-mutated rhIL-32θ induced the polarization to M1-like macrophages through the MAPK (p38) and NF-κB (p65/p50) pathways.

A novel therapeutic anti-CD55 monoclonal antibody inhibits the proliferation and metastasis of colorectal cancer cells

  • SO HEE DHO;EUN HA CHO;JI YEON LEE;SO-YOUNG LEE;SUNG HEE JUNG;LARK KYUN KIM;JAE CHEONG LIM
    • Oncology Letters
    • /
    • 제42권6호
    • /
    • pp.2686-2693
    • /
    • 2019
  • In recent years, efforts to treat cancer by improving the immune function of patients have received a great deal of attention. As part of the immune system, complement is also under such evaluation. Among the many components of the complement system, complement decay accelerating factor (CD55 or DAF) is known to inhibit complement-mediated cell lysis. However, little is known about the role of CD55 in terms of cancer therapy. The present study aimed to demonstrate that increased levels of CD55 are strongly correlated with the progression of colorectal cancer. A novel CD55 chimeric monoclonal antibody was developed that may boost the immune response, thereby suppressing cancer. The CD55 antibody treatment activated complement and therefore suppressed the proliferation, invasion and migration of colorectal cancer cells. This tumoricidal activity is partly explained by the inflammatory response via the activation of proinflammatory cytokines. In addition, the CD55 antibody treatment synergistically enhanced the tumoricidal activity of 5-FU in colorectal cancer cells, suggesting that combined treatment may be a better strategy in colorectal cancer therapy.

뇌신경교세포(腦神經膠細胞) 집단(集團)의 발생(發生)과 이동(移動)에 대한 방사선(放射線) 자기법적(自記法的) 관찰 II. 뇌(腦) 외배엽성(外胚葉性) 신경교세포(神經膠細胞)의 분열(分裂)과 이동(移動)에 대하여 (Radioautographical observations of development and appearance of glia cells in brain II. Division and migration of ectodermal glial cell in the brain)

  • 곽수동
    • 대한수의학회지
    • /
    • 제32권4호
    • /
    • pp.489-496
    • /
    • 1992
  • The division, distribution and migration of the macroglial cells in the juvenile mouse brain were investigated with the radioautography. Forty mice (ICR) were randomly subdivided into two groups. The twenty mice from group 1 were weighing initially 5 to 6g, aged 10 to 12 days and were sacrificied at 2 hrs, 2, 3, 5, 7, 10, 15 and 20 days after a single intraperitoneal injection of $^3H$-thymichine ($4{\mu}$ Ci/g of body weight). Twenty mice from group 2 were weighing intially 2.5 to 5g, aged 3 to 8 days and were sacrificed at 2 hrs, 2, 3, 5. 7, 10, 15 and 20 days after a single($4{\mu}$ Ci/g of body weight) and/or after intraperitoneal repeated injections($2{\mu}$ Ci/g of body weight/interval) at 2, 3 and 5 days after the first injection. The brain preparations were processed for autoradiogrouphy using Kodak NTB-3 emulsion following development in Kodak D-19, fixation in Kodak fixer, and then stained with cresyl echt violet or hematoxylin counterstain. The labeling index of the ectodermal glial cells in the subependymal layers of the lateral ventricles (SLLV), corpus callosum (CC), molecular layer of the neocortex (MLN ), inner layer except the molecular layer in the neocortex (ILN) and medulla of the cerebrum (MC) were invested. 1. Labeling cells appeared from 2 hour and some of them sustained in the 20 day after injection. In the single injection group, the peak of the labeling index reached a 7.6% at 3 day, 3.6% at 7 day, 3.3% at 2 day, 5.0% at 3 day and 2.3% at 2 day from the SLLV. CC, MLN, ILN and MC, respectively. In the repeated injecton group, the peak of the labeling index reached a 32.0 at 7 day, 11.0% at 10 day, 89% at 7 day, 16.0% at 10 day and 10.8% at 15 day from the SLLV, CC, MLN, ILM and MC, respectively. 2 The glial cells of the SLLV were recognized as to be migrated into the CC and to be not or less to be into the MC and ILN but to be not into the MLN. Glial cell aggregates in the neocotex and MC were recognized as to be proliferated and then disappeared in the itself regions.

  • PDF

상악 구개측 중앙부에 매복된 과잉치 (MESIODENS IN THE VAULT OF THE PALATE)

  • 민성진;김성오;이제호;곽지윤;최병재;최형준
    • 대한소아치과학회지
    • /
    • 제32권4호
    • /
    • pp.670-674
    • /
    • 2005
  • 과잉치는 치배 형성기에 정상 치판의 과도한 증식의 결과로 발생하며 산발적일 수도 있고 유전적일 수도 있다 발생 빈도는 $1{\sim}3%$이며, 2:1의 비율로 남아에게 호발한다. 주로 상악 전방부에서 많이 발견되며 매복, 영구치의 위치 이상, 정중부 이개, 낭종, 비강으로의 맹출 등과 같은 다양한 합병증을 나타낼 수도 있다. 상악 전방부에서 발견되어지는 과잉치는 치축방향에 따라 위치가 결정되며 상악 전방부 과잉치의 1/3정도는 역위 매복되어 맹출의 가능성이 없지만, 치낭의 치관 부위가 정상적인 관계로 존재하는 한 과잉치의 이동이 일어날 수 있다. 치아의 이동은 경구개, 소구치 부위, 비강까지도 일어날 수 있다. 또한 전상악 수직고경의 성장으로 시간이 지남에 따라 외과적 접근이 어려워질 수 있다. 이에 본 두 증례에서는 역위 매복된 상악 전방부의 과잉치가 구개 측 중앙부까지 이동된 것을 발견하여 외과적으로 제거하였다.

  • PDF

Cyclic Phytosphingosine-1-Phosphate Primed Mesenchymal Stem Cells Ameliorate LPS-Induced Acute Lung Injury in Mice

  • Youngheon Park;Jimin Jang;Jooyeon Lee;Hyosin Baek;Jaehyun Park;Sang-Ryul Cha;Se Bi Lee;Sunghun Na;Jae-Woo Kwon;Seok-Ho Hong;Se-Ran Yang
    • International Journal of Stem Cells
    • /
    • 제16권2호
    • /
    • pp.191-201
    • /
    • 2023
  • Background and Objectives: O-cyclic phytosphingosine-1-phosphate (cP1P) is a synthetic chemical and has a structure like sphingosine-1-phosphate (S1P). S1P is known to promote cell migration, invasion, proliferation, and anti-apoptosis through hippocampal signals. However, S1P mediated cellular-, molecular mechanism is still remained in the lung. Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are characterized by excessive immune response, increased vascular permeability, alveolar-peritoneal barrier collapse, and edema. In this study, we determined whether cP1P primed human dermal derived mesenchymal stem cells (hdMSCs) ameliorate lung injury and its therapeutic pathway in ALI mice. Methods and Results: cP1P treatment significantly stimulated MSC migration and invasion ability. In cytokine array, secretion of vascular-related factors was increased in cP1P primed hdMSCs (hdMSCcP1P), and cP1P treatment induced inhibition of Lats while increased phosphorylation of Yap. We next determined whether hdMSCcP1P reduce inflammatory response in LPS exposed mice. hdMSCcP1P further decreased infiltration of macrophage and neutrophil, and release of TNF-α, IL-1β, and IL-6 were reduced rather than naïve hdMSC treatment. In addition, phosphorylation of STAT1 and expression of iNOS were significantly decreased in the lungs of MSCcP1P treated mice. Conclusions: Taken together, these data suggest that cP1P treatment enhances hdMSC migration in regulation of Hippo signaling and MSCcP1P provide a therapeutic potential for ALI/ARDS treatment.

Anti-Angiogenic Activity of Acalycixenolide E, a Novel Marine Natural Product from Acallycigorgia inermis

  • Kwon, Ho-Jeong;Kim, Jin-Hee;Jung, Hye-Jin;Kwon, Yong-Guen;Kim, Min-Young;Rho, Jung-Rae;Shin, Jong-Heon
    • Journal of Microbiology and Biotechnology
    • /
    • 제11권4호
    • /
    • pp.656-662
    • /
    • 2001
  • Angiogenesis is known as a crucial process in the growth and spreading of tumor cells. Accordingly, the effective inhibition of this process would appear to be a promising way to cure angiogenesis-related diseases, including cancer. This study demonstrates that acalycixenolide E (AX-E) from the marine organism Acalycigorgia inermis exhibits a potent anti-angiogenic activity both in vitro and in vivo. AX-E inhibits the bFGF-induced proliferation of HUVECs in a dose dependent manner, along with the bFGF-induced migration, invasion, and tube formation of HUVECs. Moreover, AX-E potently inhibits the in vivo neovascularization of the chorioallantoic membranes (CAMs) of growing chick embryos. interestingly, AX-E suppresses the expression of metalloproteases 2 and 9, yet shows no effect on their activities. The novel chemical structure and potent anti-angiogenic activity of AX-E will be of great value in elucidating the molecular mechanism of angiogenesis as well as in the development of a novel anti-angiogenic drug.

  • PDF

FZD6 expression is negatively regulated by miR-199a-5p in human colorectal cancer

  • Kim, Bong-Kyu;Yoo, Hye-In;Kim, Injung;Park, Jongkeun;Yoon, Sungjoo Kim
    • BMB Reports
    • /
    • 제48권6호
    • /
    • pp.360-366
    • /
    • 2015
  • Colorectal cancer (CRC), the third most common cancer worldwide, also has the highest rate of cancer-related morbidity and mortality. WNT signaling is initiated by binding of WNT to various receptors, including frizzleds (FZDs), and plays a critical role in CRC and other tumor development by regulating proliferation, differentiation, migration, apoptosis, and polarity. Among the members of the FZD family, FZD6 is broadly expressed in various tissues, and its overexpression has been reported in several cancers, suggesting an important role in cancer development. In this study, we investigated the expression of FZD6 in patients with CRC and found it to be increased in tumors, as compared to paired adjacent non-tumor tissues. Additionally, we found that FZD6 expression was negatively regulated by miR199a5p in CRC cells. These results suggest that overexpression of FZD6, mediated by reduced expression of miR-199a-5p, may play an important role in the development of CRC. [BMB Reports 2015; 48(6): 360-366]

Upregulation of Fas in epithelial ovarian cancer reverses the development of resistance to Cisplatin

  • Fan, Yang;Wang, Long;Han, Xuechuan;Liu, Xueqin;Ma, Hongyun;Ding, Yonghui
    • BMB Reports
    • /
    • 제48권1호
    • /
    • pp.30-35
    • /
    • 2015
  • This study was to investigate the role of Fas in the development of Cisplatin-resistant ovarian cancer. On the cellular level, Fas expression was significantly reduced in Cisplatin resistant A2780 (A2780/CP) cells compared with A2780 cells. Fas silence with siRNA would promote tumor cell lines proliferation, facilitate tumor cell cycle transition of G1/S, prevent cell apoptosis, and promote cell migration. Expression of drug resistance gene was negatively correlated to Fas. In nude mice metastasis model of human ovarian carcinoma by subcutaneous transplantation, after Ad-Fas injected intratumorly, we found that upregulation of Fas could inhibit transplantation tumor tissue growth and reduce the expression of drug resistance gene. Our results indicated that upregulation of Fas in epithelial ovarian cancer reversed the development of resistance to Cisplatin. In conclusion, our findings suggested that Fas might act as a promising therapeutic target for improvement of the sensibility to Cisplatin in ovarian cancer.

In Vivo Anti-tumor Activity of 3-Methyl-6-allylthiopyridazine in Nude Mice Xenografted with Hep-G2 Hepatocarcinoma

  • Kwon, Soon-Kyoung;Moon, Aree
    • Biomolecules & Therapeutics
    • /
    • 제13권2호
    • /
    • pp.113-117
    • /
    • 2005
  • Organosulfur compounds have been shown to exert an anti-cancer activity. In an attempt to develop novel chemopreventive and anti-cancer agents for liver cancer, we synthesized allylthiopyridazine derivatives. We have previously shown that allylthiopyridazine derivatives exert inhibitory effects on proliferation, invasion and migration of SK-Hep-1 hepatocarcinoma cells in vitro. The in vivo anti-tumor effect of 3-methvl-6-allylthiopy-ridazine, named as K6, was also reported. In this study, we further investigated the preclinical anti-cancer efficacy of K6 for hepatocarcinoma using nude mice xenografted with Hep-G2 hepatocellular carcinoma cells. K6(20-100 mg/kg, orally administered everyday for 30 days) markedly decreased the tumor volume of Hep-G2 cell-transplanted nude mice as evidenced by ultrasonographic and plethysmogranhic analyses. The inhibitory effect on tumor volume was lower than that exerted by doxorubicin (2 mg/kg), intravenously injected) which was used as a positive control. This study shows that K6 efficiently suppresses xenograft tumor growth, revealing K6 as apotential anti-cancer agent for suppressing in vivo progression of liver cancer. Given that hepatocarcinoma is among the most prevalent and lethal malignancies and there is no effective treatment to date, our study may contribute to the potential drug development for liver cancer.