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        Impossible Differential Cryptanalysis on ESF Algorithm with Simplified MILP Model

        ( Xiaonian Wu ),( Jiaxu Yan ),( Lingchen Li ),( Runlian Zhang ),( Pinghai Yuan ),( Yujue Wang ) 한국인터넷정보학회 2021 KSII Transactions on Internet and Information Syst Vol.15 No.10

        MILP-based automatic search is the most common method in analyzing the security of cryptographic algorithms. However, this method brings many issues such as low efficiency due to the large size of the model, and the difficulty in finding the contradiction of the impossible differential distinguisher. To analyze the security of ESF algorithm, this paper introduces a simplified MILP-based search model of the differential distinguisher by reducing constrains of XOR and S-box operations, and variables by combining cyclic shift with its adjacent operations. Also, a new method to find contradictions of the impossible differential distinguisher is proposed by introducing temporary variables, which can avoid wrong and miss selection of contradictions. Based on a 9-round impossible differential distinguisher, 15-round attack of ESF can be achieved by extending forward and backward 3-round in single-key setting. Compared with existing results, the exact lower bound of differential active S-boxes in single-key setting for 10-round ESF are improved. Also, 2108 9-round impossible differential distinguishers in single-key setting and 14 12-round impossible differential distinguishers in related-key setting are obtained. Especially, the round of the discovered impossible differential distinguisher in related-key setting is the highest, and compared with the previous results, this attack achieves the highest round number in single-key setting.

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        TCP10L negatively regulates alpha-fetoprotein expression in hepatocellular carcinoma

        Suqin Shen,Huan Feng,Longjiang Liu,Wei Su,Jiaxue Wu,Long Yu 생화학분자생물학회 2020 BMB Reports Vol.53 No.8

        Alpha-fetoprotein (AFP) is one of the most commonly used and reliable biomarkers for Hepatocellular carcinoma (HCC). However, the underlying mechanism of AFP expression in HCC is poorly understood. In this study, we found that TCP10L, a gene specifically expressed in the liver, is down-regulated in HCC and that its expression inversely correlates with AFP expression. Moreover, overexpression of TCP10L suppresses AFP expression whereas knockdown of TCP10L increases AFP expression, suggesting that TCP10L might be a negative regulator of AFP. We found that TCP10L is associated with the AFP promoter and inhibits AFP promoter-driven transcriptional activity. Taken together, these results indicate that TCP10L negatively regulates AFP expression in HCC and that it could be a potential prognostic marker and therapeutic target for HCC.

      • SCIESCOPUSKCI등재

        TCP10L synergizes with MAD1 in transcriptional suppression and cell cycle arrest through mutual interaction

        ( Suqin Shen ),( Jie Zuo ),( Huan Feng ),( Meirong Bai ),( Chenji Wang ),( Youheng Wei ),( Yanhong Li ),( Yichen Le ),( Jiaxue Wu ),( Yanhua Wu ),( Long Yu ) 생화학분자생물학회 2016 BMB Reports Vol.49 No.6

        T-complex protein 10A homolog 2 (TCP10L) was previously demonstrated to be a potential tumor suppressor in human hepatocellular carcinoma (HCC). However, little is known about the molecular mechanism. MAX dimerization protein 1 (MAD1) is a key transcription suppressor that is involved in regulating cell cycle progression and Myc-mediated cell transformation. In this study, we identified MAD1 as a novel TCP10L-interacting protein. The interaction depends on the leucine zipper domain of both TCP10L and MAD1. TCP10L, but not the interaction-deficient TCP10L mutant, synergizes with MAD1 in transcriptional repression, cell cycle G1 arrest and cell growth suppression. Mechanistic exploration further revealed that TCP10L is able to stabilize intracellular MAD1 protein level. Consistently, the MAD1-interaction-deficient TCP10L mutant exerts no effect on stabilizing the MAD1 protein. Taken together, our results strongly indicate that TCP10L stabilizes MAD1 protein level through direct interaction, and they cooperatively regulate cell cycle progression. [BMB Reports 2016; 49(6): 325-330]

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