Proteins of the small ubiquitin-related modifier (SUMO) family are conjugated to proteins to regulate such cellular processes as nuclear transport, transcription, chromosome segregation and DNA repair. Recently, numerous insights into regulatory mechanisms of the SUMO modification pathway have emerged. Although SUMO-conjugating enzymes can discriminate between SUMO targets, many substrates possess characteristics that facilitate their modification. Other post-translational modifications also regulate SUMO conjugation, suggesting that SUMO signalling is integrated with other signal transduction pathways. A better understanding of SUMO regulatory mechanisms will lead to improved approaches for analysing the function of SUMO and substrate conjugation in distinct cellular pathways.

The SUMO pathway: emerging mechanisms that shape specificity, conjugation and recognition.

Polo-like kinase 1 (Plk1) overexpression has been shown to occur in a wide range of tumors, prompting research and development of Plk1 inhibitors as a means of cancer treatment. This review discusses recent advances in the development of Plk1 inhibitors for cancer management. Plk1 inhibition has been shown to cause mitotic block and apoptosis of cells with higher mitotic index and therefore higher Plk1 expression. The potential of Plk1 inhibitors as cancer therapeutics has been widely investigated. However, a complete understanding of Plk1 biology/mechanism is yet to be fully achieved. Resistance to certain chemotherapeutic drugs has been linked to Plk1 overexpression, and Plk1-mediated mitotic events such as microtubule rearrangement have been found to reduce the efficacy of chemotherapeutic agents. The Plk1 inhibitor volasertib has shown considerable promise in clinical studies, having reached phase III trials. However, preclinical success with Plk1 inhibitors has not translated well into clinical success. In our view, combined therapies targeting other relevant pathways together with Plk1 may be vital to combat issues observed with monotherapy, especially resistance. In addition, research should also be directed toward understanding the mechanisms of Plk1 and designing additional next generations of specific, potent Plk1 inhibitors to target cancer. Mol Cancer Ther; 15(7); 1427-35. ©2016 AACR.

/pdf/plk1-inhibitors-in-cancer-therapy-from-laboratory-to-clinics-31ozblybik.pdf

Plk1 Inhibitors in Cancer Therapy: From Laboratory to Clinics.

Tumor suppressor genes cooperate with each other in tumors. Three important tumor suppressor proteins, retinoblastoma (Rb), p53, phosphatase, and tensin homolog deleted on chromosome ten (PTEN) are functionally associated and they regulated by post-translational modification (PTMs) as well. PTMs include phosphorylation, SUMOylation, acetylation, and other novel modifications becoming growing appreciated. Because most of PTMs are reversible, normal cells use them as a switch to control the state of cells being the resting or proliferating, and PTMs also involve in cell survival and cell cycle, which may lead to abnormal proliferation and tumorigenesis. Although a lot of studies focus on the importance of each kind of PTM, further discoveries shows that tumor suppressor genes (TSGs) form a complex “network” by the interaction of modification. Recently, there are several promising strategies for TSGs for they change more frequently than carcinogenic genes in cancers. We here review the necessity, characteristics, and mechanisms of each kind of post-translational modification on Rb, p53, PTEN, and its influence on the precise and selective function. We also discuss the current antitumoral therapies of Rb, p53 and PTEN as predictive, prognostic, and therapeutic target in cancer.

/pdf/regulating-tumor-suppressor-genes-post-translational-47uw48ts0o.pdf

Regulating tumor suppressor genes: post-translational modifications.

Cell cycle checkpoints activated by DNA double-strand breaks (DSBs) are essential for the maintenance of the genomic integrity of proliferating cells. Following DNA damage, cells must detect the break and either transiently block cell cycle progression, to allow time for repair, or exit the cell cycle. Reversal of a DNA-damage-induced checkpoint not only requires the repair of these lesions, but a cell must also prevent permanent exit from the cell cycle and actively terminate checkpoint signalling to allow cell cycle progression to resume. It is becoming increasingly clear that despite the shared mechanisms of DNA damage detection throughout the cell cycle, the checkpoint and its reversal are precisely tuned to each cell cycle phase. Furthermore, recent findings challenge the dogmatic view that complete repair is a precondition for cell cycle resumption. In this Commentary, we highlight cell-cycle-dependent differences in checkpoint signalling and recovery after a DNA DSB, and summarise the molecular mechanisms that underlie the reversal of DNA damage checkpoints, before discussing when and how cell fate decisions after a DSB are made.

The same, only different - DNA damage checkpoints and their reversal throughout the cell cycle.

Targeting Polo-Like Kinases: A Promising Therapeutic Approach for Cancer Treatment.

Plk1-mediated Phosphorylation of Topors Regulates p53 Stability

Cdc2-mediated Phosphorylation of CLIP-170 Is Essential for Its Inhibition of Centrosome Reduplication

Based on the versatility and effectiveness of the siamese neural network, the technology of unmanned aerial vehicle visual object tracking has found widespread application in various fields including military reconnaissance, intelligent transportation, and visual positioning. However, due to complex factors, such as occlusions, viewpoint changes, and interference from similar objects during UAV tracking, most existing siamese neural network trackers struggle to combine superior performance with efficiency. To tackle this challenge, this paper proposes a novel SiamSTM tracker that is based on Slight Aware Enhancement Transformer and Multiple matching networks for real-time UAV tracking. The SiamSTM leverages lightweight transformers to encode robust target appearance features while using the Multiple matching networks to fully perceive response map information and enhance the tracker’s ability to distinguish between the target and background. The results are impressive: evaluation results based on three UAV tracking benchmarks showed superior speed and precision. Moreover, SiamSTM achieves over 35 FPS on NVIDIA Jetson AGX Xavier, which satisfies the real-time requirements in engineering.

/pdf/slight-aware-enhancement-transformer-and-multiple-matching-15tw9x2c.pdf

Slight Aware Enhancement Transformer and Multiple Matching Network for Real-Time UAV Tracking

Topors is a DNA topoisomerase I- and p53-binding protein, and mainly functions as a p53 regulator. Accumulating evidence also supports the notion that Topors plays the role as a negative regulator of cell growth, and possibly as a tumor suppressor. Here, we demonstrated that Topors is also involved in normal mitotic progression, since Topors depletion delays mitotic entry and affects mitotic progression. Furthermore, Topors is degradated in response to the activation of the spindle checkpoint. Significantly, Polo-like kinase 1 (Plk1)-associated phosphorylation of Topors at S718 is essential for nocodazole-induced degradation of Topors.

Plk1 phosphorylation of Topors is involved in its degradation

Siamese network-based trackers satisfy the balance between performance and efficiency for visual tracking. However, they do not have enough robustness to handle the challenges of target occlusion and similar objects. In order to improve the robustness of the tracking algorithm, this paper proposes visual tracking with FPN based on Transformer and response map enhancement. In this paper, a feature pyramid structure based on Transformer is designed to encode robust target-specific appearance features, as well as the response map enhanced module to improve the tracker’s ability to distinguish object and background. Extensive experiments and ablation experiments are conducted on many challenging benchmarks such as UAV123, GOT-10K, LaSOT and OTB100. These results show that the tracking algorithm we proposed in this paper can effectively improve the tracking robustness against the challenges of target occlusion and similar object, and thus improve the precision rate and success rate of the tracking algorithm.

/pdf/visual-tracking-with-fpn-based-on-transformer-and-response-26tzvntq.pdf

Visual Tracking with FPN Based on Transformer and Response Map Enhancement

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