11 results about "Tumor suppressor proteins" patented technology

The invention provides a chelating agent for use in a method of treating cancer in a subject, wherein said cancer has a resistance to an anti-cancer therapeutic agent. Further, the invention provides a chelating agent for use in a method of sensitizing a subject for an anti-cancer treatment and / or counteracting a resistance to an anti-cancer therapeutic agent, wherein the method restores or re-activates a tumor suppressor protein function that preferably was impaired due to aberrant tumor suppressor protein folding. The invention also provides a pharmaceutical composition comprising a 2,3-Dimercapto-1-propanesulfonic acid (DMPS) or DMSA, preferably miaDMSA, and a pharmaceutically acceptable excipient; wherein the DMPS is present in a dose of 40-12000 mg.

A method of obtaining cell derived vesicles comprising an active wild-type p53 is disclosed. The method comprising: (i) isolating cell derived vesicles from a biological sample comprising cells; and (ii) treating the cell derived vesicles with a DNA damaging agent, or the method comprising: (i) treating cells with a DNA damaging agent; and (ii) isolating cell derived vesicles from a biological sample comprising the cells. A proteinaceous preparation comprising cell derived vesicles and a pharmaceutical composition comprising the proteinaceous preparation are also disclosed. Methods of treating a disease, disorder or condition associated with a mutant or a nonfunctional p53 protein and methods of inducing apoptosis of a target cell comprising a mutant or a nonfunctional p53 protein are also disclosed.

The present invention discloses an intelligent responsive fusion polypeptide (HPVP-02) targeting HPV E6 / E7 protein and its application in the treatment of cervical cancer. The amino acid sequence of the polypeptide is shown in SEQ ID NO.1. It is composed of a dual-targeting module (specifically binding to HPV E6 / E7 protein), a pH response module (H5E5 sequence), an immune activation module (PD-1 / PD-L1 inhibitory peptide) and a self-assembly module (amphiphilic nanostructure), and each module is connected in series through a flexible connecting peptide. HPVP-02 responsively disassembles in the acidic microenvironment of the tumor, efficiently penetrates the cell membrane, degrades E6 / E7 protein through the ubiquitin-proteasome pathway, restores the function of the host tumor suppressor protein p53 / pRb, and simultaneously blocks the PD-1 / PD-L1 pathway to activate the anti-tumor immune response. The fusion polypeptide of the present invention has the advantages of targeting precision, low toxicity and synergistic treatment, providing an innovative treatment strategy for HPV-related tumors.

The invention is based on in vitro transcribed or in vitro synthesized RNA compounds for a translation of tumor suppressor proteins in subjects suffering from a proliferative disease such as cancer. The invention provides the RNA compounds, as well as compositions for their delivery or administration to subjects. The invention in some embodiments provides novel avenues for treating chemotherapy resistant cancer diseases.

The invention relates to the field of promoting tumor radiotherapy sensitization by targeted induction of gene expression, in particular to novel application of cancer suppressor protein LZTS3, namely application of up-regulated LZTS3 gene in preparation of lung cancer radiotherapy sensitizer drugs. According to the invention, lung cancer cells H1299 and A549 are used as examples for research, and the influence of the LZTS3 gene on the lung cancer cells is researched through RNA interference (RNAi) silent LZTS3 gene. Researches find that expression of LZTS3 is knocked down in H1299 and A549 cells, the multiplication capacity of lung cancer cells is remarkably enhanced, the number of gamma-H2AX focuses induced by ionizing radiation (IR) is reduced, the number of RAD51 focuses induced by IR is increased, and then the application of the up-regulation LZTS3 gene in preparation of tumor radiotherapy sensitizing drugs is provided. The purpose of up-regulating the expression level of the LZTS3 gene is achieved by knocking out beta-Trcp through lipidosome-mediated small interfering RNA, so that the sensitivity of tumor cells to radiotherapy is enhanced.

The invention discloses an intelligent responsive fusion polypeptide (HPVP-02) of a targeted HPV (human papillomavirus) E6 / E7 protein and application of the intelligent responsive fusion polypeptide in treatment of cervical cancer. The amino acid sequence of the polypeptide is as shown in SEQ ID NO.1, the polypeptide is composed of a dual-targeting module (specifically bound with HPV E6 / E7 protein), a pH response module (H5E5 sequence), an immune activation module (PD-1 / PD-L1 inhibitory peptide) and a self-assembly module (amphiphilic nanostructure), and all the modules are connected in series through flexible connecting peptides. The HPVP-02 is subjected to responsive disassembly in a tumor acidic microenvironment, efficiently penetrates through a cell membrane, degrades E6 / E7 protein through a ubiquitin-proteasome pathway, recovers the host cancer suppressor protein p53 / pRb function, blocks a PD-1 / PD-L1 pathway and activates anti-tumor immune response. The fusion polypeptide has the advantages of targeting accuracy, low toxicity and synergistic treatment, and provides an innovative treatment strategy for HPV-related tumors.

This invention is based on in vitro transcription RNA compounds or in vitro synthetic RNA compounds for the translation of tumor suppressor proteins in subjects suffering from proliferative diseases such as cancer. The invention provides RNA compounds and compositions for their delivery or administration to subjects.

The present invention belongs to the field of biomedicine and specifically relates to a polypeptide that targets and blocks the binding of TRIM25 to the BRD7 protein and its application. Based on the PRYSPRY domain (439 aa-630 aa), the minimal binding region of TRIM25 and BRD7 proteins, the present invention screened and obtained a blocking peptide TB16 that can specifically block the binding of TRIM25 and BRD7 proteins, thereby inhibiting the ubiquitination and degradation of BRD7 and increasing the stability of the BRD7 tumor suppressor protein. The polypeptide drug TB16 described in the present invention can effectively inhibit the proliferation of breast cancer, nasopharyngeal cancer, ovarian cancer, lung cancer, and liver cancer cells, as well as the growth of breast cancer tumors in vivo. It has excellent activity against solid tumors and is expected to become a new targeted anti-tumor drug.

The present disclosure relates generally to Retinoblastoma (Rb1) protein targeting 1, 2, 4-thiadiazolidin-3, 5-dione compounds, wherein the Rb1 protein is a known tumor suppressor protein, and methods of use thereof. In some aspects, the present disclosure relates to using such Rb1 protein targeting compounds to treat cancer or other hyperproliferative diseases, such as pancreatic cancer.

The present disclosure relates to compounds according to Formula (I), Formula (I) or a pharmaceutically acceptable salt and / or solvate thereof, compositions including such compounds, and methods useful for treating, preventing, and / or ameliorating a CDK4 and / or CDK6-mediated disorder, disease, or condition (e.g., cancer such as breast cancer) in a subject.

The application belongs to the technical field of biological medicine, and particularly relates to a tumor acidity response functional polypeptide capable of targeting and activating p53 and application thereof. The amino acid sequence of the polypeptide is shown as SEQ ID NO. 1. The application first designs and expresses the tumor acidity response functional polypeptide Trx-AAN-pHLIP-NLS-PMI (TApNP) capable of targeting and activating the tumor suppressor protein p53, and comprehensively evaluates the physical and chemical characteristics, intracellular internalization, nuclear uptake and anti-tumor activity of the polypeptide. The results show that in a weak acid environment, the TApNP can deliver PMI into cells and guide it to the cell nucleus, and effectively inhibit the proliferation of tumor cells.