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  • Open Access

    ARTICLE

    A Well Productivity Model for Multi-Layered Marine and Continental Transitional Reservoirs with Complex Fracture Networks

    Huiyan Zhao1, Xuezhong Chen1, Zhijian Hu2,*, Man Chen1, Bo Xiong3, Jianying Yang1

    FDMP-Fluid Dynamics & Materials Processing, Vol.20, No.6, pp. 1313-1330, 2024, DOI:10.32604/fdmp.2024.048840

    Abstract Using the typical characteristics of multi-layered marine and continental transitional gas reservoirs as a basis, a model is developed to predict the related well production rate. This model relies on the fractal theory of tortuous capillary bundles and can take into account multiple gas flow mechanisms at the micrometer and nanometer scales, as well as the flow characteristics in different types of thin layers (tight sandstone gas, shale gas, and coalbed gas). Moreover, a source-sink function concept and a pressure drop superposition principle are utilized to introduce a coupled flow model in the reservoir. A… More > Graphic Abstract

    A Well Productivity Model for Multi-Layered Marine and Continental Transitional Reservoirs with Complex Fracture Networks

  • Open Access

    ARTICLE

    Knockdown of SLC34A2 Inhibits Hepatocellular Carcinoma Cell Proliferation and Invasion

    Yanhua Li*1, Xia Chen†1, Hong Lu*

    Oncology Research, Vol.24, No.6, pp. 511-519, 2016, DOI:10.3727/096504016X14719078133483

    Abstract The gene solute carrier family 34 (sodium phosphate), member 2 (SLC34A2), is a member of the SLC34 family. Increasing evidence suggests that SLC34A2 is involved in the development of many human carcinomas. However, its role in hepatocellular carcinoma (HCC) is still unclear. Therefore, in this study we investigated the role of SLC34A2 in HCC and explored the underlying mechanism. We found that the expression of SLC34A2 is upregulated in HCC cell lines. Knockdown of SLC34A2 obviously inhibited HCC cell proliferation, migration/invasion, and the epithelial–mesenchymal transition (EMT) phenotype. Furthermore, knockdown of SLC34A2 significantly inhibited the expression More >

  • Open Access

    ARTICLE

    Knockdown of Collagen Triple Helix Repeat Containing-1 Inhibits the Proliferation and Epithelial-to-Mesenchymal Transition in Renal Cell Carcinoma Cells

    Xue-fei Jin, Hai Li, Shi Zong, Hong-yan Li

    Oncology Research, Vol.24, No.6, pp. 477-485, 2016, DOI:10.3727/096504016X14685034103716

    Abstract Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of More >

  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA uc.338 by siRNA Inhibits Cellular Migration and Invasion in Human Lung Cancer Cells

    Xuexin Gao*, Xuezhen Gao, Chao Li*, Yukun Zhang*, Lei Gao

    Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

    Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in More >

  • Open Access

    ARTICLE

    Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

    Liu Feng*†, Wang Wei*, Zhang Heng, Han Yantao, Wang Chunbo

    Oncology Research, Vol.24, No.5, pp. 315-325, 2016, DOI:10.3727/096504016X14666990347590

    Abstract REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, More >

  • Open Access

    ARTICLE

    TIPE2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Prostate Cancer Cells by Inhibiting PI3K/Akt Signaling Pathway

    Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, Yuan-wei Li

    Oncology Research, Vol.24, No.5, pp. 305-313, 2016, DOI:10.3727/096504016X14666990347437

    Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer More >

  • Open Access

    ARTICLE

    TIPE2 Inhibits Hypoxia-Induced Wnt/β-Catenin Pathway Activation and EMT in Glioma Cells

    Zhi-jun Liu*1, Hong-lin Liu*1, Hai-cun Zhou, Gui-cong Wang*

    Oncology Research, Vol.24, No.4, pp. 255-261, 2016, DOI:10.3727/096504016X14666990347356

    Abstract Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-α-induced protein 8 (TNFAIP8, TIPE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was More >

  • Open Access

    ARTICLE

    IGF-I Induces Epithelial-to-Mesenchymal Transition via the IGF-IR–Src– MicroRNA-30a–E-Cadherin Pathway in Nasopharyngeal Carcinoma Cells

    Ruoyu Wang*†, Heming Li, Xuefen Guo, Zhe Wang, Shanshan Liang, Chengxue Dang*

    Oncology Research, Vol.24, No.4, pp. 225-231, 2016, DOI:10.3727/096504016X14648701447931

    Abstract Recurrence and distant metastasis are the most common cause of therapeutic failure in nasopharyngeal carcinoma (NPC) patients. Insulin-like growth factor I (IGF-I) can induce epithelial-to-mesenchymal transition (EMT) in many epithelial tumors; however, whether IGF-I can enhance NPC metastasis by EMT and the mechanisms remain unclear. Herein, we have identified that IGF-I could induce EMT and enhance migration ability in NPC cell lines. Furthermore, both Src inhibitor and microRNA-30a (miR-30a) inhibitor reversed IGF-I-induced EMT, suggesting the involvement of an IGF-IR–Src–miR-30a–E-cadherin pathway in IGF-Iinduced EMT in NPC cell lines. Overall, the results of the present study may More >

  • Open Access

    ARTICLE

    Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells

    Mei-han Liu*, Shao-min Shi, Kai Li, En-qi Chen*

    Oncology Research, Vol.24, No.3, pp. 181-187, 2016, DOI:10.3727/096504016X14635761799038

    Abstract PFTK1 (PFTAIRE protein kinase 1), also named CDK14 (cyclin-dependent kinase 14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is highly expressed in several malignant tumors. However, the role of PFTK1 in the progression of non-small cell lung cancer (NSCLC) is still elusive. In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of More >

  • Open Access

    ARTICLE

    Downregulation of CREB Promotes Cell Proliferation by Mediating G1/S Phase Transition in Hodgkin Lymphoma

    Fangjin Lu*†, Ying Zheng, Paul Owusu Donkor*, Peng Zou§, Ping Mu

    Oncology Research, Vol.24, No.3, pp. 171-179, 2016, DOI:10.3727/096504016X14634208142987

    Abstract The cyclic-AMP response element-binding protein (CREB), a well-known nuclear transcription factor, has been shown to play an essential role in many cellular processes, including differentiation, cell survival, and cell proliferation, by regulating the expression of downstream genes. Recently, increased expression of CREB was frequently found in various tumors, indicating that CREB is implicated in the process of tumorigenesis. However, the effects of CREB on Hodgkin lymphoma (HL) remain unknown. To clarify the role of CREB in HL, we performed knockdown experiments in HL. We found that downregulation of CREB by short hairpin RNA (shRNA) resulted… More >

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