Manjari Kundu's research while affiliated with National Institutes of Health and other places

Publications (5)

Article
Background: TRAIL induces apoptosis in many preclinical cancer models including breast cancers and has been extensively studied as a potential cancer therapeutic. However, its efficacy in clinical trials is limited, suggesting an unknown modulatory mechanism responsible for lack of TRAIL activity in vivo. Here, we describe that TRAIL treatment elic...
Article
TRAIL induces apoptosis in many preclinical cancer models including breast cancers and has been extensively studied as a potential cancer therapeutic. However, its efficacy in clinical trials is limited, suggesting that there are unknown modulatory mechanisms responsible for its lack of TRAIL activity in vivo. We hypothesized that TRAIL treatment e...
Article
Full-text available
Breast cancer is the most frequently diagnosed malignancy worldwide and the leading cause of cancer mortality in women. Despite the recent development of new therapeutics including targeted therapies and immunotherapy, triple-negative breast cancer remains an aggressive form of breast cancer, and thus improved treatments are needed. In recent decad...
Article
Full-text available
The tumor necrosis factor (TNF) superfamily member TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells via death receptor (DR) activation with little toxicity to normal cells or tissues. The selectivity for activating apoptosis in cancer cells confers an ideal therapeutic characteristic to TRAIL, which has led to the dev...
Article
Full-text available
Mitochondria are multifaceted organelles which are important for bioenergetics, biosynthesis, and signaling in metazoans. Mitochondrial functions are frequently altered in cancer to promote both the energy and the necessary metabolic intermediates for biosynthesis required for tumor growth. Cancer stem cells (CSC) contribute to chemotherapy resista...

Citations

... This research area is rapidly advancing and holds great promise for the treatment of cancer and infections. While the authors are no experts in this field, we recommend several innovative reviews and articles produced over the past 10 years on CLPP-modulating drug compounds [215][216][217][218][219][220][221][222][223][224][225][226][227][228][229][230][231][232][233] and relevant structure/binding studies [45, [234][235][236][237][238][239][240][241][242][243][244] for further reading. A better understanding of CLPXP-dependent UPRmt will also help clarify how extra-mitochondrial signals (such as extruded mt-dsRNA, perhaps mtRNA-G4, and associated ribonucleoproteins) trigger responses of the nucleus and the endoplasmic reticulum UPR, a basic research field where mechanisms are investigated in yeast and nematodes but are poorly defined in mammals at present [41, [245][246][247][248][249][250]. ...
... Moreover, cleaved caspase-3/7, a key executioner caspase from mitochondria [43], was signi cantly higher in 3Dspheroids treated with the combinatorial therapy than in the controls ( Fig. 7E and Supplementary Fig. S7D). To further con rm that the combinatorial treatment induced cell death, we quanti ed viability, cytotoxicity, and apoptosis induction with or without the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-uoromethyl ketone (Z-VAD-FMK) [44]. The combinatorial treatment suppressed cell viability and induced cytotoxicity as well as cleaved caspase-3/7 luminescence ( Fig. 7F and Supplementary Fig. S7E). ...
... This research area is rapidly advancing and holds great promise for the treatment of cancer and infections. While the authors are no experts in this field, we recommend several innovative reviews and articles produced over the past 10 years on CLPP-modulating drug compounds [215][216][217][218][219][220][221][222][223][224][225][226][227][228][229][230][231][232][233] and relevant structure/binding studies [45, [234][235][236][237][238][239][240][241][242][243][244] for further reading. A better understanding of CLPXP-dependent UPRmt will also help clarify how extra-mitochondrial signals (such as extruded mt-dsRNA, perhaps mtRNA-G4, and associated ribonucleoproteins) trigger responses of the nucleus and the endoplasmic reticulum UPR, a basic research field where mechanisms are investigated in yeast and nematodes but are poorly defined in mammals at present [41, [245][246][247][248][249][250]. ...