• IMMUNE NETWORK
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• 제21권5호
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• pp.37.1-37.17
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• 2021

Hepatitis B virus X (HBx) protein has been reported as a key protein regulating the pathogenesis of HBV-induced hepatocellular carcinoma (HCC). Recent evidence has shown that HBx is implicated in the activation of autophagy in hepatic cells. Nevertheless, the precise molecular and cellular mechanism by which HBx induces autophagy is still controversial. Herein, we investigated the molecular and cellular mechanism by which HBx is involved in the TRAF6-BECN1-Bcl-2 signaling for the regulation of autophagy in response to TLR4 stimulation, therefore influencing the HCC progression. HBx interacts with BECN1 (Beclin 1) and inhibits the association of the BECN1-Bcl-2 complex, which is known to prevent the assembly of the pre-autophagosomal structure. Furthermore, HBx enhances the interaction between VPS34 and TRAF6-BECN1 complex, increases the ubiquitination of BECN1, and subsequently enhances autophagy induction in response to LPS stimulation. To verify the functional role of HBx in liver cancer progression, we utilized different HCC cell lines, HepG2, SK-Hep-1, and SNU-761. HBx-expressing HepG2 cells exhibited enhanced cell migration, invasion, and cell mobility in response to LPS stimulation compared to those of control HepG2 cells. These results were consistently observed in HBx-expressed SK-Hep-1 and HBx-expressed SNU-761 cells. Taken together, our findings suggest that HBx positively regulates the induction of autophagy through the inhibition of the BECN1-Bcl-2 complex and enhancement of the TRAF6-BECN1-VPS34 complex, leading to enhance liver cancer migration and invasion.

• Asian Pacific Journal of Cancer Prevention
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• 제17권12호
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• pp.5173-5177
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• 2016

Acute myeloid leukemia (AML), one of the most prevalent leukemia types in adults, demonstrates great heterogeneity in molecular and clinical terms. Hence, there is a necessity to the mechanisms involved in AML generation in order to determine optimal treatment. This cross sectional study aimed to assess changes in BECN1 gene expression in with blood samples from 30 AML patients, compared with samples from 15 healthy persons. RNA was extracted and cDNA was synthesized and Real Time PCR applied to determine BECN1 gene expression. The results showed no significant differences in BECN1 gene expression between patients with AML and normal controls (P > 0.05). It appears that expression of BECN1 does not play a significant role in genesis of AML leukemia.

• 정보처리학회논문지C
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• 제13C권4호
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• pp.441-446
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• 2006

최근, IP 기반 인터넷 트래픽의 폭발적인 증가로 인하여 인터넷의 백본 네트워크로서 광 WDM 네트워크가 주목을 받고 있다. 광 버스트 교환(OBS)은 WDM 네트워크에서 사용될 효과적인 교환 기술로서 제안되었다. 광 버스트 교환은 대역폭을 효율적으로 사용하고 광 버퍼가 불필요하다는 크게 두 가지의 이점을 가지고 있다. 그러나, 광 버스트 교환은 네트워크 내에서 광 버스트가 충돌하는 문제점을 가지고 있다. 우회 라우팅(deflection routing)이 이 문제를 해결하는 하나의 방법으로 제안되었다. 본 논문에서는 우회 라우팅을 사용하는 환경에서 버스트 손실을 최소화하는 새로운 라우팅 방법을 제안한다. 또한 새로운 라우팅 알고리즘을 이용하여 QoS 제어 방법을 제안한다. 마지막으로, 컴퓨터 시뮬레이션을 통하여 제안 방법의 유효성을 보인다.

• 대한전자공학회:학술대회논문집
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• 대한전자공학회 2004년도 하계종합학술대회 논문집(1)
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• pp.241-244
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• 2004

In recent years, WDM networks have received much attention as the Internet backbone networks because of the explosive growth of the Internet IP-based traffic. The Optical Burst Switching (OBS) has been proposed as an effective optical switching technology in the WDM networks. OBS has the advantages in 1) the high usage rate of the bandwidth, and 2) no necessity of optical buffer. However OBS has the burst-contention problem in the networks. The deflection routing is proposed as one of means to solve this problem. In this paper, we propose a new routing method of using deflection routing. In addition. we propose a QoS/CoS control method using a new routing algorithm. Finally, we show the variety of the proposed methods by computer simulations.

• 한국정보처리학회논문지
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• 제2권6호
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• pp.927-936
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• 1995

ATM 포럼에서는 버스트 특성이 높고 그 크기를 예측하기 힘든 트래픽 특성을 가진 ABR 트래픽을 새로이 정의하였다. 이 트래픽은 지연보다 손실에 더 민감한 특성을 가지 므로 셀의 손실을 최소화하여 패킷을 재전송하는 경우를 최소화하는 것이 바람직하다. ATM 포럼에서는 ABR트래픽 제어를 위해 율기반 (rate-based)제어 방식인 EPRCA알고리 즘을 채택하였다. 본 논문에서는 이 EPRCA 알고리즘과 BECN, BP 등과 같은 피이드백 제어 방법을 조합한 형태의 제어 방식을 제안한다. 이러한 조합형태의 제어 방식은 ABR 트래픽을 좀더 효율적으로 제어할 수 있고 파라미터 값을 적절히 제어함으로써 효율성을 더욱 높일 수 있음을 시뮬레이션을 통하여 보인다.

• Journal of Korean Neurosurgical Society
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• 제65권2호
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• pp.236-244
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• 2022

Objective : To evaluate the interactions among differentially expressed autophagy and mitophagy markers in subarachnoid hemorrhage (SAH) patients with delayed cerebral ischemia (DCI). Methods : The expression data of autophagy and mitophagy-related makers in the cerebrospinal fluid (CSF) cells was analyzed by real-time reverse transcription-polymerase chain reaction and Western blotting. The markers included death-associated protein kinase (DAPK)-1, BCL2 interacting protein 3 like (BNIP3L), Bcl-1 antagonist X, phosphatase and tensin homolog-induced kinase (PINK), Unc-51 like autophagy activating kinase 1, nuclear dot protein 52, and p62. In silico functional analyses including gene ontology enrichment and the protein-protein interaction network were performed. Results : A total of 56 SAH patients were included and 22 (38.6%) of them experienced DCI. The DCI patients had significantly increased mRNA levels of DAPK1, BNIP3L, and PINK1, and increased expression of BECN1 compared to the non-DCI patients. The most enriched biological process was the positive regulation of autophagy, followed by the response to mitochondrial depolarization. The molecular functions ubiquitin-like protein ligase binding and ubiquitin-protein ligase binding were enriched. In the cluster of cellular components, Lewy bodies and the phagophore assembly site were enriched. BECN1 was the most connected gene among the differentially expressed markers related to autophagy and mitophagy in the development of DCI. Conclusion : Our study may provide novel insight into mitochondrial dysfunction in DCI pathogenesis.

• Journal of Chest Surgery
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• 제30권4호
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• pp.432-436
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• 1997

심낭의 원발성 악성 중피종은심종양보다더 드문 질환으로 비록 와그너에 의해 1870년 처음 기술되었지만, 중피종이라는 용어는 아담에 의해 1910년 처음 사용되었다 대부분의 보고된 예들은 부검에 의해 진단 되었다. 생존시 진단은 세계적으로도 단지 40례 정도에 불과하다. 코헨에 의하면 부검한 예 중 500,000례에서 2.2례의 빈도를 보고하였다. 최근의 고찰된 분석을 보면 생존시 진단율은 전체 예 중 19-25%정도이다. 이 보고서는 심낭의 악성 중피종의 본 흉부외과학교실의 경험한 1예이다.

• Molecules and Cells
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• 제38권2호
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• pp.138-144
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• 2015

Raloxifene is a selective estrogen receptor modulator (SERM) that binds to the estrogen receptor (ER), and exhibits potent anti-tumor and autophagy-inducing effects in breast cancer cells. However, the mechanism of raloxifene-induced cell death and autophagy is not well-established. So, we analyzed mechanism underlying death and autophagy induced by raloxifene in MCF-7 breast cancer cells. Treatment with raloxifene significantly induced death in MCF-7 cells. Raloxifene accumulated GFP-LC3 puncta and increased the level of autophagic marker proteins, such as LC3-II, BECN1, and ATG12-ATG5 conjugates, indicating activated autophagy. Raloxifene also increased autophagic flux indicators, the cleavage of GFP from GFP-LC3 and only red fluorescence-positive puncta in mRFP-GFP-LC3-expressing cells. An autophagy inhibitor, 3-methyladenine (3-MA), suppressed the level of LC3-II and blocked the formation of GFP-LC3 puncta. Moreover, siRNA targeting BECN1 markedly reversed cell death and the level of LC3-II increased by raloxifene. Besides, raloxifene-induced cell death was not related to cleavage of caspases-7, -9, and PARP. These results indicate that raloxifene activates autophagy-dependent cell death but not apoptosis. Interestingly, raloxifene decreased the level of intracellular adenosine triphosphate (ATP) and activated the AMPK/ULK1 pathway. However it was not suppressed the AKT/mTOR pathway. Addition of ATP decreased the phosphorylation of AMPK as well as the accumulation of LC3-II, finally attenuating raloxifene-induced cell death. Our current study demonstrates that raloxifene induces autophagy via the activation of AMPK by sensing decreases in ATP, and that the overactivation of autophagy promotes cell death and thereby mediates the anti-cancer effects of raloxifene in breast cancer cells.

• 한국표면공학회지
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• 제31권1호
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• pp.34-44
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• 1998

Stainless steel is being used widely lor various purposes due to its good corrosion resistance. There has becn much research to produce colored stainless sterl by several methods. In this experiment, we coated TixN film on the SUS304 substrate with thc DC magnetron sputtering system and studied the internal structurc and adhesive strength of the films as a function of the coating conditions. Before lhe specimen was coated, a sputter etching was very effective in removing the$\delta$ Fe(BCC) phase as well as the contaminant and oxide layer as well as increasing rotghness. Five-stage failure mode appeared with increased scratch load with the TIN films coated on the SUS304 in this manner ; tensile failure-,conformal failure-,buckling failure->chipping failurc and spalling Failure. When the failure was terminated at the initial stage, the film will have good adhesion. But, if syalling failure has occurred at the initial scratch, then the adhesion will be poor. The interlayer between thc coated film and thc substratc was homogeneously adhcsive when the $\gamma'-Fe_4N$ phase wasn't detected in the XRD analysis and the adhesive strength only was reduced by surPace defects. But, when the ,$\gamma'-Fe_4N$N phasc was detected in the XRD analysis, the adhesive strength was very poor.

• 한국동물생명공학회지
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• 제37권3호
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• pp.169-175
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• 2022

Bovine mammary epithelial (MAC-T) cells are commonly used to study mammary gland development and mastitis. Lipopolysaccharide is a major bacterial cell membrane component that can induce inflammation. Autophagy is an important regulatory mechanism participating in the elimination of invading pathogens. In this study, we evaluated the mechanism underlying bacterial mastitis and mammary cell death following lipopolysaccharide treatment. After 24 h of 50 ㎍/mL lipopolysaccharide treatment, a significant decrease in the proliferation rate of MAC-T cells was observed. However, no changes were observed upon treatment of MAC-T cells with 10 ㎍/mL of lipopolysaccharide for up to 48 h. Thus, upon lipopolysaccharide treatment, MAC-T cells exhibit dose-dependent effects of growth inhibition at 10 ㎍/mL and death at 50 ㎍/mL. Treatment of MAC-T cells with 50 ㎍/mL lipopolysaccharide also induced the expression of autophagy-related genes ATG3, ATG5, ATG10, ATG12, MAP1LC3B, GABARAP-L2, and BECN1. The autophagy-related LC3A/B protein was also expressed in a dose-dependent manner upon lipopolysaccharide treatment. Based on these results, we suggest that a high dose of bacterial infection induces mammary epithelial cell death related to autophagy signals.