RegRSA: Using Registers as Buffers to Resist Memory Disclosure Attacks

Part 8: Sidechannel AnalysisInternational audienceMemory disclosure attacks, such as cold-boot attacks and DMA attacks, allow attackers to access all memory contents, therefore introduce great threats to plaintext sensitive data in memory. Register-based and cache-based schemes have been used to implement RSA securely, at the expense of decreased performance. In this paper, we propose another concept named register buffer, which makes use of all available registers as secure data buffer, no matter scalar registers or vector registers. The plaintext sensitive data only appear in register buffer. Based on this concept, we finish a security implementation of 2048-bit RSA called RegRSA, to defeat against memory disclosure attacks. The 1024-bit Montgomery multiplication in RegRSA runs entirely in register buffer, by performing computations using scalar instructions and registers, maintaining intermediate variables in vector registers. Due to the size limitation of register buffer, several variables out of Montgomery multiplications are spilled into memory. RegRSA encrypts these variables with AES before saving in memory. Furthermore, RegRSA employs a windowing method and the CRT speed-up to accelerate RSA, and minimizes the data exchange between registers and memory to reduce the workload of AES encryption/decryption. The evaluation on Intel Haswell i7-4770R shows that, the performance of RegRSA achieves a factor of 0.74 compared to the regular RSA implementation in OpenSSL and is much greater than PRIME, the existing register-based scheme for 2048-bit RSA. Moreover, RegRSA allows multiple instances to run on a multi-core CPU simultaneously, which makes it more practical for the real-world applications

Rac3 induces a molecular pathway triggering breast cancer cell aggressiveness: differences in MDA-MB-231 and MCF-7 breast cancer cell lines.

International audienceBACKGROUND: Rho GTPases are involved in cellular functions relevant to cancer. The roles of RhoA and Rac1 have already been established. However, the role of Rac3 in cancer aggressiveness is less well understood. METHODS: This work was conducted to analyze the implication of Rac3 in the aggressiveness of two breast cancer cell lines, MDA-MB-231 and MCF-7: both express Rac3, but MDA-MB-231 expresses more activated RhoA. The effect of Rac3 in cancer cells was also compared with its effect on the non-tumorigenic mammary epithelial cells MCF-10A. We analyzed the consequences of Rac3 depletion by anti-Rac3 siRNA. RESULTS: Firstly, we analyzed the effects of Rac3 depletion on the breast cancer cells' aggressiveness. In the invasive MDA-MB-231 cells, Rac3 inhibition caused a marked reduction of both invasion (40%) and cell adhesion to collagen (84%), accompanied by an increase in TNF-induced apoptosis (72%). This indicates that Rac3 is involved in the cancer cells' aggressiveness. Secondly, we investigated the effects of Rac3 inhibition on the expression and activation of related signaling molecules, including NF-κB and ERK. Cytokine secretion profiles were also analyzed. In the non-invasive MCF-7 line; Rac3 did not influence any of the parameters of aggressiveness. CONCLUSIONS: This discrepancy between the effects of Rac3 knockdown in the two cell lines could be explained as follows: in the MDA-MB-231 line, the Rac3-dependent aggressiveness of the cancer cells is due to the Rac3/ERK-2/NF-κB signaling pathway, which is responsible for MMP-9, interleukin-6, -8 and GRO secretion, as well as the resistance to TNF-induced apoptosis, whereas in the MCF-7 line, this pathway is not functional because of the low expression of NF-κB subunits in these cells. Rac3 may be a potent target for inhibiting aggressive breast cancer