• Anatomy and Cell Biology
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• 제56권4호
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• pp.409-414
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• 2023

Botulinum neurotoxin (BoNT) injection for the treating plunged nose, post-rhinopasty and hyaluronic filler migration is common procedures in clinical settings. However, the lack of thorough anatomical understanding makes it difficult to locate the nose region muscles. The anatomical considerations concerned with BoNT injection into the nasalis, levator labii superioris alaeque, and depressor septi nasi muscles were reviewed in this study. The injection spots have been presented for the nasalis, levator labii superioris alaeque, and depressor septi nasi muscles, with the recommended injection technique for each muscle. We have suggested the ideal injection sites in association with outer anatomical landmarks of the nose region. Moreover, these proposals would support a more accurate procedure of BoNT injection in relieving plunged nose, preventing post-rhinoplasty deviation, and migration of the hyaluronic acid filler.

• Asian Pacific Journal of Cancer Prevention
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• 제13권11호
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• pp.5653-5657
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• 2012

Objectives: To investigate the effect of glycopeptide-preferring polypeptide GalNAc transferase 1 (ppGalNAc T1 ) targeted RNA interference (RNAi) on the growth and migration of human bladder carcinoma EJ cells in vitro and in vivo. Methods: DNA microarray assays were performed to determine ppGalNAc Ts(ppGalNAc T1-9) expression in human bladder cancer and normal bladder tissues. We transfected the EJ bladder cancer cell line with well-designed ppGalNAc T1 siRNA. Boyden chamber and Wound healing assays were used to investigate changes of shppGalNAc T1-EJ cell migration. Proliferation of shppGalNAc T1-EJ cells in vitro was assessed using [3H]-thymidine incorporation assay and soft agar colony formation assays. Subcutaneous bladder tumors in BALB/c nude mice were induced by inoculation of shppGalNAc T1-EJ cells and after inoculation diameters of tumors were measured every 5 days to determine gross tumor volumes. Results: ppGalNAc T1 mRNA in bladder cancer tissues was 11.2-fold higher than in normal bladder tissues. When ppGalNAc T1 expression in EJ cells was knocked down through transfection by pSUPER-shppGalNAc T1 vector, markedly reduced incorporation of [3H]-thymidine into DNA of EJ cells was observed at all time points compared with the empty vector transfected control cells. However, ppGalNAc T1 knockdown did not significantly inhibited cell migration (only 12.3%). Silenced ppGalNAc T1 expression significantly inhibited subcutaneous tumor growth compared with the control groups injected with empty vector transfected control cells. At the end of observation course (40 days), the inhibitory rate of cancerous growth for ppGalNAc T1 knockdown was 52.5%. Conclusion: ppGalNAc T1 might be a potential novel marker for human bladder cancer. Although ppGalNAc T1 knockdown caused no remarkable change in cell migration, silenced expression significantly inhibited proliferation and tumor growth of the bladder cancer EJ cell line.

• 한국환경생태학회지
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• 제29권5호
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• pp.681-692
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• 2015

월동기간 동안 월동조류의 생리 및 영양학적 상태는 이후 번식지로의 이동성공과 번식성공에 영향을 줄 수 있음은 잘 알려져 있다. 그러나 환경적 요인들이 월동기간 동안 어떻게 몸 상태에 영향을 주어 장기적으로 이동과 번식에 영향을 주는지에 대해서는 아직까지 잘 알려져 있지 않다. 본 연구는 월동기간 동안 온도변화와 월동지에서의 인간 활동에 따른 방해가 개체수준에서의 월동하는 조류의 생활사에 미치는 영향과 번식지로의 이동 및 잠재적 번식 성공에 미치는 영향을 알아보기 위해 동적상태의존 월동 생활사 모델을 개발하였다. 모델에 사용된 지수는 월동개체군에 대한 연구가 잘 수행되어 있는 철원의 두루미 자료를 이용하였다. 모델은 온도 변화나 인간의 방해요인의 영향이 생존과 번식지로의 이동을 위한 에너지 축적 그리고 누적된 스트레스의 감소를 위한 자원 분배에 영향을 주는 것으로 예측하였다. 특히 월동지에 도래한 두루미 몸무게의 회복률은 기온변화가 적고 방해요인의 영향이 낮을수록 빨랐으며, 체내의 누적 스트레스는 기온변화가 크고 방해요인의 영향이 높을수록 회복속도가 낮을 것으로 예측되었다. 또한 월동지의 취식지를 공유하는 다른 종의 밀도가 높을수록 두루미의 몸무게 회복률이 낮은 것으로 예측되었다. 끝으로 모델의 예측된 결과를 통해 월동지에서의 월동조류 보전전략에 대해 고찰하였다.

• Radiation Oncology Journal
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• 제33권4호
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• pp.328-336
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• 2015

Purpose: Past studies have reported that S-allylcysteine (SAC) inhibits the migration and invasion of cancer cells through the restoration of E-cadherin, the reduction of matrix metalloproteinase (MMP) and Slug protein expression, and inhibition of the production of reactive oxygen species (ROS). Furthermore, evidence is emerging that shows that ROS induced by radiation could increase Met activation. Following on these reports of SAC and Met, we investigated whether SAC could suppress Met activation. Materials and Methods: Wound healing, invasion, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium (MTT), soft agar colony forming, western blotting, and gelatin zymography assays were performed in the human nasopharyngeal cancer cell lines HNE1 and HONE1 treated with SAC (0, 10, 20, or 40 mM) and hepatocyte growth factor (HGF). Results: This study showed that SAC could suppress the migration and invasion of HNE1 and HONE1 cell lines by inhibiting p-Met. An increase of migration and invasion induced by HGF and its decrease in a dose dependent manner by SAC in wound healing and invasion assays was observed. The reduction of p-Met by SAC was positively correlated with p-focal adhesion kinase (p-FAK) and p-extracellular related kinase (p-ERK in both cell lines). SAC reduced Slug, MMP2, and MMP9 involved in migration and invasion with the inhibition of Met-FAK signaling. Conclusion: These results suggest that SAC inhibited not only Met activation but also the downstream FAK, Slug, and MMP expression. Finally, SAC may be a potent anticancer compound for nasopharyngeal cancer treated with radiotherapy.

• International Journal of Oral Biology
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• 제43권3호
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• pp.161-169
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• 2018

We previously demonstrated that epidermal growth factor (EGF) enhances cell migration and invasion of breast cancer cells in a SMAD ubiquitination regulatory factor 1 (SMURF1)-dependent manner and that SMURF1 induces degradation of ${\beta}-catenin$ in C2C12 cells. However, the relationship between EGF-induced SMURF1 and ${\beta}-catenin$ expression in breast cancer cells remains unclear. So, we investigated if EGF and SMURF1 regulate ${\beta}-catenin$ expression in MDAMB231 human breast cancer cells. When MDAMB231 cells were incubated with EGF for 24, 48, and 72 hours, EGF significantly increased expression levels of SMURF1 mRNA and protein while suppressing expression levels of ${\beta}-catenin$ mRNA and protein. Overexpression of SMURF1 downregulated ${\beta}-catenin$ mRNA and protein, whereas knockdown of SMURF1 increased ${\beta}-catenin$ expression and blocked EGF-induced ${\beta}-catenin$ downregulation. Knockdown of ${\beta}-catenin$ enhanced cell migration and invasion of MDAMB231 cells, while ${\beta}-catenin$ overexpression suppressed EGF-induced cell migration and invasion. Furthermore, knockdown of ${\beta}-catenin$ enhanced vimentin expression and decreased cytokeratin expression, whereas ${\beta}-catenin$ overexpression decreased vimentin expression and increased cytokeratin expression. These results suggest that EGF downregulates ${\beta}-catenin$ in a SMURF1-dependent manner and that ${\beta}-catenin$ downregulation contributes to EGF-induced cell migration and invasion in MDAMB breast cancer cells.

• 생약학회지
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• 제45권3호
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• pp.256-261
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• 2014

Bee venom (BV) therapy has been used as a traditional medicine to treat a variety of conditions, such as arthritis, back pain, cancerous tumors, and skin diseases. However, regulatory effects of BV on tumor necrosis factor (TNF)-${\alpha}$-induced HaCaT cell migration or anti-inflammatory have not been explored. In the present study, we investigated the effects of BV on HaCaT cell migration and anti-inflammation. HaCaT cell migration was evaluated by wound-healing assay. The pro-inflammatory cytokines such as TNF-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-8 were examined by ELISA or Western blotting. BV treatment led to an increase in migration of HaCaT cells for 24 and 48 h. Especially, 10 ng/ml of BV were significantly increased HaCaT cell migration. Also, BV suppressed the secretion of TNF-${\alpha}$, IL-$1{\beta}$, and IL-8 in culture medium with HaCaT cells. In addition, Western blot results demonstrate that BV suppressed the expression of TNF-${\alpha}$ and IL-$1{\beta}$, in HaCaT cells. Especially, 1 or 10 ng/ml of BV markedly decreased the expression of pro-inflammatory cytokines. These results demonstrate the potential of BV for the prevention of skin inflammation induced by TNF-${\alpha}$.

• 동의생리병리학회지
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• 제36권1호
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• pp.1-6
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• 2022

The tuber of Pinellia ternata (Thunb.) Brei (TPT) used in traditional Oriental medicine for the treatment of cough, sputum, vomiting, and insomnia, possesses antioxidant, antibacterial, and anti-inflammatory effects. Although recent studies have reported the anticancer effects of TPT in several cancer cells, it is still unclear whether TPT regulates tumor-associated macrophage (TAM) characterized by the immunosuppressive M2 macrophage phenotype. Our results showed that the ethanol extract of TPT (ETPT) suppressed the migration of RAW264.7 mouse macrophage cells and THP-1 human monocytes differentiated into macrophages towards the conditioned media (CM) collected from lung cancer cells, suggesting that ETPT would attenuate the recruitment of macrophages into tumors. In addition, ETPT suppressed the interleukin (IL)-4 or IL-6-induced M2 macrophage polarization in RAW264.7 cells. ETPT treatment not only downregulated the mRNA expression of M2 macrophage markers including arginase-1, mannose receptor C type 1 (MRC-1), and IL-10, but also inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and STAT6, general regulators of M2 macrophage polarization. Finally, the transwell assay results showed that the CM from M2-polarized RAW264.7 cells increased the migration of mouse lewis lung carcinoma (LLC) cells, while those from RAW264.7 cells co-treated with ETPT and IL-6 significantly reduced the migration of LLC cells. Taken together, our observations clearly demonstrate that ETPT suppressed the cancer cell migration by regulating macrophage recruitment and M2 macrophage polarization.

• 디지털융복합연구
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• 제14권5호
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• pp.117-123
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• 2016

다문화사회가 되면서 과연 외국인 이주노동자들의 정주화방지 원칙을 고수하는 것이 옳은 판단인가 하는 질문이 본 연구의 출발점이었다. 외국인이주노동자들의 정주화방지 원칙은 비단 이주노동자들의 인권이나 정서적 측면에서의 고려가 아니라, 우리가 좀 더 냉정하게 정주화방지 원칙에 대해서 고찰해 볼 필요가 있다. 산업수요를 개선하여 3D업종의 비중을 낮추어가야 한다는 반론도 있을 수 있으나, 3D산업을 완전히 없애는 것이 불가능하다면, 우리사회가 대안을 마련해야 한다는 점에서 이주노동자는 그 대안이 될 수 있다. 정주화방지원칙은 우선, 다문화사회의 흐름과 배치될 뿐 아니라, 이주노동자들이 우리나라에서 연마한 관련기술이 전파되거나 공유할 수 있는 기회를 차단하는 것이다. 또한 고령화사회가 되면서 이주노동자의 정주화는 부족한 젊은 노동력을 공급할 수 있는 적절한 채널이 될 수 있음을 명심해야 할 것이다. 이러한 실용적인 측면에서의 이유 외에도 정주화방지원칙은 모든 인간은 평등하고 인격적으로 존엄한 존재라는 인권의 측면에서 볼 때, 정주화방지로 인해 발생하는 이주노동자들이 겪게되는 불평등한 상황을 좀 더 따뜻한 시선으로 바라볼 수 있어야 한다는 점에서도 수정이 되어야 한다고 본다.

• BMB Reports
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• 제51권10호
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• pp.532-537
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• 2018

Prostaglandin $E_2$ ($PGE_2$), a major product of cyclooxygenase-2 (COX-2), plays an important role in the carcinogenesis of many solid tumors, including colorectal cancer. Because $PGE_2$ functions by signaling through $PGE_2$ receptors (EPs), which regulate tumor cell growth, invasion, and migration, there has been a growing amount of interest in the therapeutic potential of targeting EPs. In the present study, we investigated the role of EP4 on the effectiveness of cordycepin in inhibiting the migration and invasion of HCT116 human colorectal carcinoma cells. Our data indicate that cordycepin suppressed lipopolysaccharide (LPS)-enhanced cell migration and invasion through the inactivation of matrix metalloproteinase (MMP)-9 as well as the down-regulation of COX-2 expression and $PGE_2$ production. These events were shown to be associated with the inactivation of EP4 and activation of AMP-activated protein kinase (AMPK). Moreover, the EP4 antagonist AH23848 prevented LPS-induced MMP-9 expression and cell invasion in HCT116 cells. However, the AMPK inhibitor, compound C, as well as AMPK knockdown via siRNA, attenuated the cordycepin-induced inhibition of EP4 expression. Cordycepin treatment also reduced the activation of CREB. These findings indicate that cordycepin suppresses the migration and invasion of HCT116 cells through modulating EP4 expression and the AMPK-CREB signaling pathway. Therefore, cordycepin has the potential to serve as a potent anti-cancer agent in therapeutic strategies against colorectal cancer metastasis.

• Asian Pacific Journal of Cancer Prevention
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• 제16권8호
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• pp.3213-3222
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• 2015

Background: Cancer metastasis depends on cell motility which is driven by cycles of actin polymerization and depolymerization. Reactive oxygen species (ROS) and metabolic oxidative stress have long been associated with cancer. ROS play a vital role in regulating actin dynamics that are sensitive to oxidative modification. The current work aimed at studying the effects of sub-lethal metabolic oxidative stress on actin cytoskeleton, focal adhesion and cell migration. Materials and Methods: T47D human breast cancer cells were treated with 2-deoxy-D-glucose (2DG), L-buthionine sulfoximine (BSO), or doxorubicin (DOX), individually or in combination, and changes in intracellular total glutathione and malondialdehyde (MDA) levels were measured. The expression of three major antioxidant enzymes was studied by immunoblotting, and cells were stained with fluorescent-phalloidin to evaluate changes in F-actin organization. In addition, cell adhesion and degradation ability were measured. Cell migration was studied using wound healing and transwell migration assays. Results: Our results show that treating T47D human breast cancer cells with drug combinations (2DG/BSO, 2DG/DOX, or BSO/DOX) decreased intracellular total glutathione and increased oxidized glutathione, lipid peroxidation, and cytotoxicity. In addition, the drug combinations caused a reduction in cell area and mitotic index, prophase arrest and a decreased ability to form invadopodia. The formation of F-actin aggregates was increased in treated T47D cells. Moreover, combination therapy reduced cell adhesion and the rate of cell migration. Conclusions: Our results suggest that exposure of T47D breast cancer cells to combination therapy reduces cell migration via effects on metabolic oxidative stress.