Cancer chemotherapy is generally associated with many severe adverse effects. Many cancer studies are currently focused on repurposing conventional non-toxic anti-parasite drugs for cancer treatment. Since cancer cells and parasites have many features in common, some anti-parasite drugs such as benzimidazoles have been recently found to possess the anti-cancer activity. Benzimidazoles act against cancer by inhibiting tubulin polymerization, inducing cancer cell apoptosis, arresting cell cycle and over-generating reactive oxygen specimen. In this review, we summarize the anticancer features of these drugs in recent investigations, lead to reconsideration of benzimidazoles as a family of anti-cancer chemotherapeutics with non-toxicity or low toxicity to the normal cells and tissues. We particularly highlight the recent progresses using nanoformulations for enhanced cancer therapy and provide our prospects in the future research.

Peripheral nerve injury is a serious and disabling disease prevalent in the world. It caused by trauma is often accompanied with soft tissue injuries, fractures, infections, etc., and can cause permanent damage. The treatment methods of peripheral nerve injury mainly include traditional microsurgical repair, neurotrophic drug treatment, as well as cuttingedge nerve conduit treatment, nerve stimulation, cell therapy, etc. However, more than 30% of patients with peripheral nerve injury still have poor recovery, including partial loss or complete loss of motor and/or sensory function, muscle atrophy，chronic pain and severe disability, among can lead to permanent disease. Phenolic compounds are secondary metabolites which is the most abundant in plants, consisting of an aromatic ring and one or more hydroxyl substituents, the main groups including flavonoids, phenolic acids, tannins, stilbene and lignans. A lot of studies have shown that natural phenolic compounds have various properties, such as antioxidant, anti-infective, anticancer, anti-inflammatory, etc., and have broad applications in the prevention of heart disease, cancer, diabetes, oxidative stress-related diseases, and neuroprotection prospect. This review discusses the potential applications and molecular mechanisms of natural phenolic compounds its polymer derivatives in the treatment of peripheral nerve injury.

Green innovation, driven by China's new development concept, plays a crucial role in high-quality economic development. In line with the green development trend, businesses increasingly prioritize whether their corporate environmental responsibilities (CER) can effectively enhance corporate green innovation (CGI) levels. This paper examines the influence and mechanism of CER on CGI using a dynamic perspective, drawing from 1,640 manually-collected panel data of Shanghai and Shenzhen A-share listed companies between 2010 and 2017. The primary findings indicate that the impact of CER on CGI possesses phase-specific characteristics and a dual effect of "crowding in" and "crowding out." The current phase of CER negatively affects green innovation, while the lag phase has a positive effect. CER's impact on various CGI types is heterogeneous: specifically, it follows an "inverted-N" trajectory (inhibition-promotion-inhibition) for "strategic green innovation" and has a promotional effect on "substantive green innovation," which is stronger and has a longer time lag. The mechanism analysis reveals that financing constraints play a critical mediating role. A heterogeneity analysis based on multiple dimensions (ownership, industry, and location) suggests that CER has a more significant driving force for CGI among state-owned firms, high-polluting industries, and enterprises in inland areas. Finally, the paper presents corresponding suggestions for government and corporate entities.

Approximately 28 million individuals in the United States face the risk of developing precancerous colonic adenomas (polyps) and potentially progressing to colorectal cancer (CRC). While a promising strategy for CRC prevention involves pharmacological intervention, such as cancer chemoprevention or interception, currently, there are no FDA-approved drugs capable of preventing the formation or progression of adenomas to adenocarcinoma. Numerous clinical, epidemiological, and preclinical studies have offered compelling evidence supporting the efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) in CRC chemoprevention. However, the prolonged use of NSAIDs is not FDA-approved due to potential life-threatening toxicities resulting from cyclooxygenase (COX) inhibition and the depletion of physiological prostaglandins. Despite indications that the COX inhibitory activity of NSAIDs may not be essential for their antineoplastic effects, the absence of a well-defined target impeded the development of derivatives that do not inhibit COX. Earlier research suggests that the inhibition of cyclic guanosine monophosphate phosphodiesterase (cGMP PDE) may be responsible, at least in part, for the antineoplastic activity of the NSAID sulindac. This could potentially offer a novel target for CRC chemoprevention. To identify the cGMP PDE isozyme(s) contributing to the antineoplastic activity of sulindac, we synthesized a chemically diverse library of over 1500 compounds, all sharing the indene scaffold of sulindac. Subsequently, we screened these compounds for their impact on cancer cell growth and PDE inhibitory activity. From this screening, a series of lead compounds emerged. These compounds lacked COX-1 and COX-2 inhibitory activity, surpassing sulindac in potency to inhibit CRC cell growth. Importantly, they demonstrated greater selectivity by not affecting normal cell growth. Through chemical optimization, we identified several development candidates that selectively inhibit PDE5 and/or PDE10. These compounds activate cGMP/PKG signaling, suppressing Wnt/β-catenin transcription. This action counters the growth advantages resulting from APC or CTNNB1 mutations, which are responsible for most human CRCs. This review delves into the scientific literature supporting PDE5 and/or PDE10 as potential targets for CRC chemoprevention or interception. Our findings suggest a promising avenue for developing drugs that may effectively intervene in the progression of colorectal cancer, offering hope for improved preventive strategies in the future.

The latent transforming growth factor-beta (TGF-β) binding protein 1 (LTBP1) has been implicated in various cellular processes, but its role in triple-negative breast cancer (TNBC) remains unclear. In this study, we investigated the impact of LTBP1 on TNBC progression and its underlying mechanisms. Analysis of online datasets revealed elevated LTBP1 mRNA expression in breast cancer tissues compared to normal adjacent tissues. Kaplan-Meier Plotter analysis indicated that high LTBP1 expression was negatively correlated with relapse-free survival (RFS), distant-metastasis free survival (DMFS), and overall survival (OS) of breast cancer patients. Additionally, LTBP1 mRNA levels were associated with chemotherapy resistance. Functional assays in TNBC cells demonstrated that LTBP1 knockdown suppressed cell proliferation, induced apoptosis, and attenuated migration and invasion. In vivo studies confirmed that LTBP1 knockdown inhibited tumor growth in a xenograft mouse model. Mechanistically, LTBP1 positively correlated with genes involved in signaling regulation and organelle organization, with significant associations to GTPase binding and the RhoA/ROCK pathway. LTBP1 knockdown reduced RhoA activity and phosphorylation of Myosin Light Chain 2 (MLC2), suggesting inhibition of the RhoA/ROCK signaling pathway. Moreover, activation of the RhoA/ROCK pathway partially rescued the effects of LTBP1 knockdown on TNBC cell proliferation, apoptosis, migration, and invasion. In conclusion, our findings suggest that LTBP1 promotes TNBC progression through activation of the RhoA/ROCK signaling pathway, highlighting its potential as a therapeutic target for TNBC.