Subgenus Bothynoptera Schaum, 1863 of the genus Parena is mainly found in Oriental region. Despite this widespread distribution, species of the subgenus Bothynoptera are poorly known in Korea. While a total of 14 species have been recorded worldwide, only 3 species have been recorded in Korea. In this study, as a revisional work of Korean known species, a pictorial key and photographs of habitus and male genitalia for each species are provided, with a newly recorded species in Korea.

The continuous use of pesticides with the same mode of action has lead to the development of insecticide resistance in the target pests. Establishing pesticide resistance management methods and effective control strategies for these pests has become an important target. Bemisia tabaci, a representative pest of greenhouse, directly affects the growth of crops at all stages of its development except eggs. It also causes indirect damage by secreting honeydew that eventually promotes sooty mold in leaves and fruits. In this study, eight insecticides with different mechanisms of action (Flonicamid, Fluxametamide, Spinetoram, Cyantraniliprole, Dinotefuran, Pyridaben, Milbemectin and Pyriproxyfen), and registered for use against cucumber B. tabaci were selected and tested for insecticide resistance. The tested populations of B. tabaci were collected from greenhouse cucumber cultivations in 12 domestic regions. The results were presented as RR (Resistance ratios), and CEI (Control efficacy index) values.

The rate of resistant pest emergence has accelerated due to the continuous use of pesticides. Therefore, it is important to formulate insecticide resistance management measures and effective control methods for pest. Bemisia tabaci, a greenhouse pest, causes direct damage to crops such as growth inhibition and leaf discoloration at all developmental stages except for eggs. It also indirectly damages plants by secreting honeydew, which covers surrounding leaves and fruits, leading to sooty mold development. In this study, eight insecticides with high usage rates, categorized by their mode of action, were selected. Samples of Bemisia tabaci were collected from six regions, and resistance analysis were conducted. The results showed that Flonicamid exhibited a resistance ratio of 8.91 in Sejong, while Pyriproxyfen showed a high resistance ratio of 63.56 in Gunwi. Fluxametamide, Spinetoram, Cyantraniliprole, Dinotefuran, Pyridaben, and Milbemectin displayed resistance ratio ranging from 0.02 to 1.14 in most regions, except for Flonicamid and Pyriproxyfen.

Porphyromonas gingivalis is a gram-negative bacteria of rod shape, and grown in an anerobic condition. It colonizes in subgingival crevice and is known as a major pathogen causing chronic periodontitis. It possesses an invasive property and replicative potential within various cell types, presumably playing an important role in modulating biological behaviors of oral cancer. However, the pathophysiology of P. gingivalis in the malignant transformation of oral cancer has not been fully understood. In this study, we aimed to investigate molecular changes of oral squamous cell carcinoma cells induced by repetitive P. gingivalis infection that clinically resembles chronic periodontitis.

Recently, the importance of inflammation in carcinogenesis has been recognized and studied extensively. As a result, a clear correlation between inflammation and carcinogenesis has been well established in some types of cancers. Despite a high prevalence of chronic periodontitis, one of the most common inflammatory diseases in the general population, there are only a few reports on the role of chronic periodontitis in oral cancer progression. In this study, we aimed to investigate genetic changes in oral cancer cells induced by repetitive Porphryomonas gingivalis infections to mimic chronic periodontitis in a clinical setting. Cells of oral squamous cell carcinoma (OSCC), the most common type of oral cancer, and P. gingivalis 381 were used for the present study. ID1 and ID3 were mRNAs of higher expression in the P. gingivalis-infected group compared to the uninfected control. These mRNAs have been regarded as important modulators participating in cancer progression. Future studies will provide an insight into the roles of the molecules we identified in oral cancer progression. Outcomes from these studies will also shed light on the significance of chronic periodontitis induced by bacterial pathogen, such as P. gingivalis, in progression of oral cancer and relevant molecular mechanisms underlying altered cancer cell behaviors.

Chronic inflammation is widely considered to predispose individuals to cancer. Microorganisms facilitate recruitment and activation of inflammatory cells and thus allow release of inflammatory mediators. These molecules can then promote accumulation of mutations, leading to tumor development in the host. Porphyromonas gingivalis, a pathogen causing chronic periodontitis, is detected in oral squamous cell carcinoma (OSCC) tissues. Considering a strong link between chronic inflammation and tumor development, functional consequences of P. gingivalis infection may include malignant transformation of the host cells. In this study, we monitored transcriptional changes induced by invasion of P. gingivalis in OSCC cells using microarrays. Our preliminary results suggest changes in a wide range of genes involved in inflammation, apoptosis and autophagy, tumor progression, and carcinogenesis. Further studies on molecular mechanisms underlying these changes will lay a useful foundation to elucidate the role of microorganism-related inflammation and for the development of preventive and therapeutic agents for oral cancer.

Metastasis consists of complex cascades and a lot of factors are involved in each step of metastasis. In recent studies, the role of epithelial-mesenchymal transition (EMT) in metastasis is suggested. EMT has a feature of epithelial cells conversing into mesenchymal cells morphologically and phenotypically, is a characteristic of malignant and metastatic cells in most cancer. The mesenchymal cells usually show more malignant phenotype, including invasion and metastasis. EMT can play an important role in metastasis of oral squamous cell carcinoma (OSCC). Although the role of Snail, slug, other transcriptional factors and E-cadherin are well known in human cancers, there are a few studies on N-cadherin and Twist expression in OSCC. The present study was aimed to analyze the expression of N-cadherin and Twist protein in OSCC from Korean patients. The immunohistochemical stain was performed using 58 primary OSCCs and 6 metastatic OSCCs, and the correlation between the expression of these proteins and clinicopathological parameters of OSCC patients was analyzed. The expression rate of high expression of N-cadherin was observed in 70.4% and Twist in 87.3% of OSCC. The expression of N-cadherin in metastatic OSCC increased than in corresponding primary OSCC (p<0.05). The spearman correlation coefficiency between N-cadherin and Twist was calculated as 0.228. The clinical factors such as lymph node metastasis and survival showed statistically significant correlation between N-cadherin expression. The expression of Twist was correlated with recurrence. In conclusion, the authors suggest that N-cadherin may play an important role in malignant behaviour of OSCC and can be considered as prognostic indicator of OSCC.

Cancer cells are often found in an ischemic condition due to the rapid outgrowth of their vascular supply, and these cells are expected to develop an increased potential for local invasive growth. Since the first steps are characterized by increased motility and invasiveness, expression of molecules involved in cellular adhesion to extracellular matrix (ECM) is increased in the process of cancer cell invasion and metastasis. In this work we explored the molecular characteristics and its regulatory mechanism of hypoxic oral squamous cell carcinoma (OSCC) cells. Our experiment identified that hypoxia increases α5 integrin protein levels through phosphoinositide 3-kinase (PI3K)/Akt pathway in OSCC cells.

Malignant tumor cells outgrow new blood vessel formation and tend to be in hypoxic state. Hypoxic cancer cells adapt to hypoxic conditions by transforming its characteristics. On the other hand, one of the most important features of cancer cells is that carcinoma cells loses its inherent epithelial phenotype and acquires mesenchymal characteristics, called as epithelial-mesenchymal transition(EMT). It has been already well known that EMT contributes to tumor invasion and metastasis. The present study investigated whether hypoxia play a major role in induction of phenotypic changes of oral squamous cell carcinoma(OSCC). Furthermore, the mechanism of EMT in oral squamous cell carcinoma cells by hypoxia has been clarified. To mimic hypoxic condition, cobalt chloride and desferoxamine, well-known hypoxic mimetic agents, were used. This study shows that hypoxia suppresses the expression of E-cadherin(epithelial marker) and increases vimentin and N-cadherin( mesenchymal markers) in OSCC. In addition, α5 integrin protein, which is a receptor for fibronectin and an important molecule for tumor invasion, is prominently induced by hypoxia.

Adherent cells, such as those found in epithelial tissues, must be physically associated with extracellular matrix (ECM)components to survive. Though stimulation by growth factors is an essential factor in cell survival, normal cells also requires cell adhesion to ECM proteins. The cessation of these anchorage-mediated signals seems to be a common mechanism to physiolog ically t erminate t he l ife cycle of t hese c ells b y apoptosis. This form o f cell death has been termed anoikis.In cancer, resistance to anoikis of cancer cell is important in invasion and metastasis. The present study investigated the intracellular mechanism involved in anoikis, especially in cells treated with epigallocatechin- 3-gallate(EGCG). To induce anoikis, cell culture plates were coated with 10 ㎍/ml poly-HEMA. A549 lung adenocarcinoma cells were grown in RPMI 1640 medium with/without 10% fetal bovine serum, and then cells were replated on cell culture dishes coated with poly-HEMA in the presence or absence of serum. On the other hand, EGFR inhibitor, PI3K inhibitor, and EGCG were treated to the anoikis status cells, in order to evaluate the factors of anoikis. The result revealed that growth factors or loss of adhesion can increase phosphorylate Akt. In addition, lack of cell adhesion fails to activate pro-apoptotic factors directly. Activity of Erk kinase depends on not only EGFR signaling but also cell adhesion. Akt activation is mainly affected by EGCG whereas Raf-1 activation is controlled by the presence of cell contact. In addition, EGCG increased the level of NFkB, whereas phophroylated PTEN and total PTEN were not different. In this report,increase of NFkB was correlated with Akt phosphorylation, suggesting that EGCG can protect cells from detachment–induced cell death through Akt activation and subsequent NFkB

Green tea, derived from the plant Camellia sinensis, is one of the most common beverages consumed worldwide. Epigallocatechin-3-gallate (EGCG) is the most abundant and bioactive polyphenolic constituent in green tea. Understanding how intracellular signaling pathways respond to EGCG may provide a clue to the difference of cell responses and basis for usefulness of EGCG as a chemopreventive and/or chemotherapeutic agent. In the present study, we tried to check whether EGCG could be a useful agent in chemotherapeutic treatment of oral squamous carcinoma. Furthermore, we investigated which signaling pathway is involved in biologic activities of EGCG. EGCG induced the cell death of oral squamous carcinoma cells. Furthermore, it increased phosphorylation of Akt in serum-strarved oral squamous carcinoma cells. But, initial increase of Akt activation did not affect cell survival. Activities of Raf-1 and Erk showed inconsistent response to EGCG treatment, but Erk phosphorylation is consistent with Raf-1 activity in YD 10B cells. These changes of Raf-1 and Erk activity in EGCG treated cells were different depending on cell line type. Supposedly, the difference of cell component may affect the Raf-1 and Erk reactivity to EGCG treatment. Akt activation by EGCG is independent on activities of PDK1 and PTEN, and expression of bax and bcl-2 proteins were not changed by EGCG treatment. Therefore, EGCG treatment did not induce the apoptosis of YD 10B cell. On the other hand, vascular adhesion molecule (VCAM) was decreased by EGCG treatment, so it is possible that decrease of VCAM can play certain role in survival and/or cell death in EGCG treated cells

Tumor cells under hypoxic conditions are often found due to the rapid outgrowth of their vascular supply, and,in order to survive hypoxia, these cells induce numerous signaling factors. Erk is an important kinase in cell survival, and its activity is regulated by Raf kinases through numerous growth factor receptors. The authors investigated Erk activation and Raf/Erk signaling using the hypoxia-mimetic agent, cobalt chloride (CoCl2), in oral squamous cell carcinoma (OSCC) cells. CoCl2 increases Erk phosphorylation in both a dose- and time-dependent manner. In addition, blocking the activation of epidermal growth factor receptor (EGFR) using PD168393 abolished Erk activation in response to CoCl2, suggesting that Erk phosphorylation by CoCl2 is dependent on EGFR.