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Nanomedicines for drug delivery and imaging-guided cancer therapy is a rapidly growing research area. The unique properties of nanomedicines have a massive potential in solving longstanding challenges of existing cancer drugs, such as poor localization at the tumor site, high drug doses and toxicity, recurrence, and poor immune response. However, inadequate biocompatibility restricts their potential in clinical translation. Therefore, advanced nanomaterials with high biocompatibility and enhance

Reported here is a molecular construct (<b>K1</b>) designed to overcome hurdles associated with delivering active drugs to heterogeneous tumor environments. Construct <b>K1</b> relies on two cancer environment triggers (GSH and H₂O₂) to induce prodrug activation. It releases an active drug form (SN-38) under conditions of both oxidative and reductive stress <i>in vitro</i>. Specific uptake of <b>K1</b> in COX-2 positive aggressive colon cancer cells (SW620 and LoVo) was see

Tissue selective targeting and specific suborganellular localization combined with an efficient pathology associated enzymatic activation of drugs in drug delivery systems may exhibit a clear advantage over conventional cancer treatment. Here, a mitochondria targeted aggregation induced emission (AIE) fluorophore further conjugated with an NAD(P)H:quinone oxidoreductase-1 (NQO1) cleavable masking unit showed preferential uptake in cancer cells and was selectively activated, resulting in bright A

Although elevated expression of CAV1/caveolin 1 is associated with the malignant progression of various human cancers, the molecular mechanism underlying its oncogenic functions is largely unknown. We found that CAV1 is frequently overexpressed in advanced colorectal tumors due to aberrant promoter CpG site hypomethylation, and its elevation is implicated in enhanced aerobic glycolysis of tumor cells. Depletion of elevated CAV1 downregulates glucose uptake, intracellular ATP level and lactate ac

PRKCDBP is a proapoptotic tumor suppressor which is commonly altered in colorectal cancer by promoter hypermethylation, and its gene transcription is directly activated by NF-κB in response to TNFα. This suggests that PRKCDBP inactivation may contribute to tumor progression by reducing cellular sensitivity to TNFα and other stresses, particularly under chronic inflammatory microenvironment.

RASSF1A is a tumor suppressor implicated in many tumorigenic processes; however, the basis for its tumor suppressor functions are not fully understood. Here we show that RASSF1A is a novel antagonist of protumorigenic RhoA activity. Direct interaction between the C-terminal amino acids (256-277) of RASSF1A and active GTP-RhoA was critical for this antagonism. In addition, interaction between the N-terminal amino acids (69-82) of RASSF1A and the ubiquitin E3 ligase Smad ubiquitination regulatory

TGF-β1 plays biphasic functions in prostate tumorigenesis, inhibiting cell growth at early stages but promoting malignant progression at later stages. However, the molecular basis for the oncogenic conversion of TGF-β1 function remains largely undefined. Here, we demonstrate that PPARδ is a direct transcription target of TGF-β1 and plays a critical role in oncogenic redirection of TGF-β1 signaling. Blockade of PPARδ induction enhances tumor cell response to TGF-β1-mediated growth inhibition, whi

Melanoma is the most threatening form of metastatic skin cancer that develops from melanocytes and causes a large majority of deaths due to poor therapeutic prognosis. It has significant limitations in treatment because it shows great resistance to chemotherapy, radiotherapy, and other therapeutic methods. A noninvasive and clinically accepted therapeutic modality, photodynamic therapy (PDT), is a promising treatment option, but it is limitedly applied for melanoma skin cancer treatment. This is

α-Lipoic acid (α-LA) is a biogenic antioxidant that has been used successfully in the treatment of diabetic polyneuropathy and its application to many oxidative stress-associated chronic diseases has increased. In this study, we investigated the effect of α-LA on colorectal cancer cell growth and its underlying mechanism. α-LA treatment resulted in a marked reduction in the growth of HCT116 colon cancer cells in a dose-dependent manner through the G1 arrest of the cell cycle and apoptosis induct

Human NAD(P)H:quinone oxidoreductase 1 (hNQO1) is overexpressed in cancer cells and associated with the drug resistance factor of cancer. The objective of this work is the development of fluorescent probes for the efficient detection of hNQO1 activity in cancer cells, which can be employed for the cancer diagnosis and therapeutic agent development. Herein, we report naphthalimide-based fluorescent probes 1 and 2 that can detect hNQO1. For hNQO1 activity, the probes showed a significant fluoresce