| 1. |
- Cheng, Dantong, et al.
(författare)
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MicroRNA-20a-5p promotes colorectal cancer invasion and metastasis by downregulating Smad4
- 2016
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Ingår i: Oncotarget. - : IMPACT JOURNALS LLC. - 1949-2553. ; 7:29, s. 45199-45213
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Tidskriftsartikel (refereegranskat)abstract
- Background: Tumor metastasis is one of the leading causes of poor prognosis for colorectal cancer (CRC) patients. Loss of Smad4 contributes to aggression process in many human cancers. However, the underlying precise mechanism of aberrant Smad4 expression in CRC development is still little known. Results: miR-20a-5p negatively regulated Smad4 by directly targeting its 3UTR in human colorectal cancer cells. miR-20a-5p not only promoted CRC cells aggression capacity in vitro and liver metastasis in vivo, but also promoted the epithelial-to-mesenchymal transition process by downregulating Smad4 expression. In addition, tissue microarray analysis obtained from 544 CRC patients clinical characters showed that miR-20a-5p was upregulated in human CRC tissues, especially in the tissues with metastasis. High level of miR-20a-5p predicted poor prognosis in CRC patients. Methods: Five miRNA target prediction programs were applied to identify potential miRNA(s) that target(s) Smad4 in CRC. Luciferase reporter assay and transfection technique were used to validate the correlation between miR-20a-5p and Smad4 in CRC. Wound healing, transwell and tumorigenesis assays were used to explore the function of miR-20a-5p and Smad4 in CRC progression in vitro and in vivo. The association between miR-20a-5p expression and the prognosis of CRC patients was evaluated by Kaplan-Meier analysis and multivariate cox proportional hazard analyses based on tissue microarray data. Conclusions: miR-20a-5p, as an onco-miRNA, promoted the invasion and metastasis ability by suppressing Smad4 expression in CRC cells, and high miR-20a-5p predicted poor prognosis for CRC patients, providing a novel and promising therapeutic target in human colorectal cancer.
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| 2. |
- Chen, Hui, et al.
(författare)
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A CORDIC-Based Architecture with Adjustable Precision and Flexible Scalability to Implement Sigmoid and Tanh Functions
- 2020
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Ingår i: IEEE International Symposium on Circuits and Systems, ISCAS 2020. - : IEEE.
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Konferensbidrag (refereegranskat)abstract
- In the artificial neural networks, tanh (hyperbolic tangent) and sigmoid functions are widely used as activation functions. Past methods to compute them may have shortcomings such as low precision or inflexible architecture that is difficult to expand, so we propose a CORDIC-based architecture to implement sigmoid and tanh functions, which has adjustable precision and flexible scalability. It just needs shift-add-or-subtract operations to compute high-accuracy results and is easy to expand the input range through scaling the negative iterations of CORDIC without changing the original architecture. We adopt the control variable method to explore the accuracy distribution through software simulation. A specific case (ARCH:(1, 15, 18), RMSE: 10(-6)) is designed and synthesized under the TSMC 40nm CMOS technology, the report shows that it has the area of 36512.78 mu m(2) and power of 12.35mW at the frequency of 1GHz. The maximum work frequency can reach 1.5GHz, which is better than the state-of-the-art methods.
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| 3. |
- Chen, Hui, et al.
(författare)
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A General Methodology and Architecture for Arbitrary Complex Number Nth Root Computation
- 2021
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Ingår i: 2021 SCAS 2021/IEEE International Symposium on Circuits and Systems. - : Institute of Electrical and Electronics Engineers (IEEE).
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Konferensbidrag (refereegranskat)abstract
- As the existing complex number Nth root computation methods are relatively discrete, we propose a general method and architecture based on coordinate rotation digital computer (CORDIC) to compute arbitrary complex number Nth root for the first time. Our method performs the tasks of computing complex modulus, complex phase angle, real Nth root, sine function and cosine function, which can be implemented by circular CORDIC, linear CORDIC and hyperbolic CORDIC. Based on these CORDICs, our proposed architecture can not only improve the hardware efficiency just through shift-add operations, but also flexibly adjust the precision and the input range of complex number Nth root. To prove its feasibility, we conduct a software simulation and implement an example circuit in hardware. Under the TSMC 28nm CMOS technology, we synthesize it and get the report that it has the area of 6561 mu m(2) and the power of 3.95mW at the frequency of 1.5GHz.
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| 4. |
- Chen, Hui, et al.
(författare)
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An Efficient Hardware Architecture with Adjustable Precision and Extensible Range to Implement Sigmoid and Tanh Functions
- 2020
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Ingår i: Electronics. - : MDPI. - 2079-9292. ; 9:10
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Tidskriftsartikel (refereegranskat)abstract
- The efficient and precise hardware implementations of tanh and sigmoid functions play an important role in various neural network algorithms. Different applications have different requirements for accuracy. However, it is difficult for traditional methods to achieve adjustable precision. Therefore, we propose an efficient-hardware, adjustable-precision and high-speed architecture to implement them for the first time. Firstly, we present two methods to implement sigmoid and tanh functions. One is based on the rotation mode of hyperbolic CORDIC and the vector mode of linear CORDIC (called RHC-VLC), another is based on the carry-save method and the vector mode of linear CORDIC (called CSM-VLC). We validate the two methods by MATLAB and RTL implementations. Synthesized under the TSMC 40 nm CMOS technology, we find that a special case AR divide VR(3,0), based on RHC-VLC method, has the area of 4290.98 mu m2 and the power of 1.69 mW at the frequency of 1.5 GHz. However, under the same frequency, AR divide VC(3) (a special case based on CSM-VLC method) costs 3196.36 mu m2 area and 1.38 mW power. They are both superior to existing methods for implementing such an architecture with adjustable precision.
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| 5. |
- Chen, Hui, et al.
(författare)
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Low-Complexity High-Precision Method and Architecture for Computing the Logarithm of Complex Numbers
- 2021
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Ingår i: IEEE Transactions on Circuits and Systems Part 1. - : Institute of Electrical and Electronics Engineers (IEEE). - 1549-8328 .- 1558-0806. ; 68:8, s. 3293-3304
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Tidskriftsartikel (refereegranskat)abstract
- This paper proposes a low-complexity method and architecture to compute the logarithm of complex numbers based on coordinate rotation digital computer (CORDIC). Our method takes advantage of the vector mode of circular CORDIC and hyperbolic CORDIC, which only needs shift-add operations in its hardware implementation. Our architecture has lower design complexity and higher performance compared with conventional architectures. Through software simulation, we show that this method can achieve high precision for logarithm computation, reaching the relative error of 10(-7). Finally, we design and implement an example circuit under TSMC 28nm CMOS technology. According to the synthesis report, our architecture has smaller area, lower power consumption, higher precision and wider operation range compared with the alternative architectures.
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| 6. |
- Chen, Hui, et al.
(författare)
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Symmetric-Mapping LUT-Based Method and Architecture for Computing X-Y-Like Functions
- 2021
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Ingår i: IEEE Transactions on Circuits and Systems Part 1. - : IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC. - 1549-8328 .- 1558-0806. ; 68:3, s. 1231-1244
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Tidskriftsartikel (refereegranskat)abstract
- We propose a new method and hardware architecture to compute the functions expressed as XY ( X and Y are arbitrary floating-point numbers), which can support arbitrary Nth root, exponential and power operations. Because of the complexity of direct computation, we usually convert it to logarithm, multiplication, and antilogarithm operations. Traditional approaches suffer from long latency, large area and high power consumption. To solve this problem, we propose a symmetric-mapping lookup table (SM-LUT) to be capable of computing log(2) x (x is an element of [1, 2]) and 2 x (x is an element of [0, 1]) simultaneously. It lays the foundation for computing XY. To further improve hardware performance of our architecture, we propose a multi-region address searcher to speed up the calculation of SM-LUT. In addition, we use an optimized Vedic multiplier to shorten the critical path and improve the efficiency of multiplication, which is included in computing X-Y. Under the TSMC 40nm CMOS technology, we design and synthesize a reference circuit to compute X-Y with a maximum relative error of 10(-3). The report shows that the reference circuit achieves the area of 14338.50 mu m(2) and the power consumption of 4.59 mW at the frequency of 1 GHz. In comparison with the state-of-the-art work under the same input range and similar precision, it saves 78.57% area and 80.42% power consumption for (N)root R computation and 82.89% area and 81.89% power consumption for R-N computation averagely. On top of that, our architecture reduces the computation latency by 62.77% averagely and has one more order of magnitude of energy efficiency than others.
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| 7. |
- Mi, Yushuai, et al.
(författare)
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miR-181a-5p promotes the progression of gastric cancer via RASSF6-mediated MAPK signalling activation
- 2017
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Ingår i: Cancer Letters. - : ELSEVIER IRELAND LTD. - 0304-3835 .- 1872-7980. ; 389, s. 11-22
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Tidskriftsartikel (refereegranskat)abstract
- We previously discovered that Ras association domain family member 6 (RASSF6) was downregulated and predicted poor prognosis in GC patients. However, the mechanisms of the down regulation of RASSF6 in GC remained unclear. Increasing evidence indicates that dysregulation of microRNAs promotes the progression of cancer through the repression of tumour suppressors. Here, we identified miR-181a-5p as a novel regulator of RASSF6 in GC. Functionally, ectopic expression or silencing of miR-181a-5p, respectively, promoted or inhibited GC cell proliferation, colony formation and cell cycle transition, as well as enhanced or prevented the invasion, metastasis of GC cells and epithelial to mesenchymal transition of GC cells in vitro and in vivo. Molecularly, miR-181a-5p functioned as an onco-miRNA by activating the RASSF6-regulated MAKP pathway. Overexpression or silencing of RASSF6 could partially reverse the effects of the overexpression or repression of miR-181a-5p on GC progress caused by activation of the MAKP pathway in vitro and in vivo. Clinically, high miR-181a-5p expression predicted poor survival in GC patients, especially combined with low RASSF6 expression. Collectively, we identified miR-181a-5p as an onco-miRNA, which acts by directly repressing RASSF6 in GC. (C) 2017 The Authors. Published by Elsevier Ireland Ltd.
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| 8. |
- Yang, Lie, et al.
(författare)
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Knockdown of PPAR δ Gene Promotes the Growth of Colon Cancer and Reduces the Sensitivity to Bevacizumab in Nude Mice Model
- 2013
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 8:4
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Tidskriftsartikel (refereegranskat)abstract
- The role of peroxisome proliferator – activated receptor- δ (PPAR δ) gene in colon carcinogenesis remains highly controversial. Here, we established nude mice xenograft model using a human colon cancer cell line KM12C either with PPAR δ silenced or normal. The xenografts in PPAR δ-silenced group grew significantly larger and heavier with less differentiation, promoted cell proliferation, increased expression of vascular endothelial growth factor (VEGF) and similar apoptosis index compared with those of PPAR δ-normal group. After treated with the specific VEGF inhibitor bevacizumab, the capacities of growth and proliferation of xenografts were decreased in both groups while still significantly higher in PPAR δ-silenced group than in PPAR δ-normal group. Administration of PPAR δ agonist significantly decreased VEGF expression in PPAR δ-normal KM12C cells but not in PPAR δ-silenced cells. These findings demonstrate that, knockdown of PPAR δ promotes the growth of colon cancer by inducing less differentiation, accelerating the proliferation and VEGF expression of tumor cells in vivo, and reduces tumor sensitivity to bevacizumab. This study indicates that PPAR δ attenuates colon carcinogenesis.
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| 9. |
- Zhao, Senlin, et al.
(författare)
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miR-4775 promotes colorectal cancer invasion and metastasis via the Smad7/TGF beta-mediated epithelial to mesenchymal transition
- 2017
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Ingår i: Molecular Cancer. - : BIOMED CENTRAL LTD. - 1476-4598. ; 16
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Tidskriftsartikel (refereegranskat)abstract
- Background: Despite advancements in the diagnosis and treatment of colorectal cancer (CRC), many patients die because of tumor metastasis or recurrence. Therefore, identifying new prognostic markers and elucidating the mechanisms of CRC metastasis and recurrence will help to improve the prognosis of the disease. As dysregulation of microRNAs is strongly related to cancer progression, the aim of this study was to identify the role of miR-4775 in the prognosis of CRC patients and the underling mechanisms involved in CRC progression. Methods: qPCR and in situ hybridization were used to evaluate the expression of miR-4775 in 544 pairs of paraffin-embedded normal and CRC tissues. Kaplan-Meier analysis with the log-rank test was used for survival analyses. Immunohistochemical staining was applied to investigate the expression of miR-4775-regulated Smad7/TGF beta pathway-associated markers. In vitro and in vivo invasion and metastasis assays were used to explore the function of miR-4775 in the progression of CRC. Results: miR-4775 was identified as a high-risk factor for CRC metastasis and recurrence, with high levels predicting poor survival among the 544 studied CRC patients. Furthermore, high miR-4775 expression promoted the invasion of CRC cells as well as metastasis and the epithelial to mesenchymal transition (EMT) via Smad7-mediated activation of TGF beta signaling both in vitro and in vivo. Downregulating miR-4775 or overexpressing Smad7 reversed the tumor-promoting roles of miR-4775/ Smad7/TGF beta in vitro and in vivo. Conclusion: miR-4775 promotes CRC metastasis and recurrence in a Smad7/TGF beta signaling-dependent manner, providing a new therapeutic target for inhibiting the metastasis or recurrence of the disease.
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