Nevertheless, a study by Yu et al. has revealed that another combination of four factors (Oct3/4, Sox2, NANOG [Nanog ho-meobox], and LIN28 [lin-28 homolog]) is also sufficient to induce pluripotent stem cells from human somatic cells, 4 indicating that more genes are involved in the establishment or maintenance of pluripotency. In this case, the therapy of HCC directing to one or several of these genes may be insufficient to achieve satisfactory efficacy. On the other hand, a recent report by Gupta et al. showed that salinomycin might selectively eliminate breast CSCs and inhibit metastasis by inducing the differentiation of CSCs. They also suggest that it is preferable to treat cancer using agents that target both the CSCs and non-CSCs, because non-CSCs might transform into CSCs and thus eradication of CSCs alone may not obtain complete regression of an established tumor. 5 Interestingly, our study indicated that HNF4 could induce the differentiation of both hepatoma cells and its CSCs. The suppression of CSCs was accompanied by the inhibition of a cluster of genes which contribute to the pluripotency of human stem cells, including-catenin, Oct3/4, SMO(smoothened homolog), Bmi, Sox2, NANOG, c-Myc, Klf4, LIN28, and ESG1 (enhancer of split groucho 1). 3 More recently, we also demonstrated that up-regulation of HNF4 remarkably ameliorated hepatic fibrosis 6 and prevented the development of HCC in rats accompanied by the revision of epithelial-mesenchymal transition (unpublished data). Thus, we believe that differentiation therapy with HNF4, a central regulator for hepatocyte differentiation, might be an ideal strategy for the treatment of human HCC. Moreover, this strategy may be extended to other cancer types through the induction of differentiation using their corresponding key transcription factors.

Black phosphorus (BP) nanomaterials have emerged as rapidly rising stars in the field of nanomedicine. In this work, BP quantum dots (BPQDs) are synthesized and their potential as photosensitizers is investigated for the first time. The BPQDs present good stability in physiological medium and no appreciable cytotoxicity. More importantly, the BPQDs can be rapidly eliminated from the body in their intact form via renal clearance due to their ultrasmall hydrodynamic diameter (5.4 nm). Both in vitro and in vivo studies indicate that the BPQDs have excellent photodynamic effect under light irradiation that can effectively generate reactive oxygen species to kill cancer cells. The BPQDs thus can serve as biocompatible and powerful photosensitizers for efficient photodynamic therapy.

We report the synthesis of two-dimensional Te nanosheets through a facile liquid exfoliation method. The as-synthesized Te nanosheets can produce reactive oxygen species under light irradiation and show high photoacoustic imaging performance due to their strong near-infrared absorbance, and can be engineered as a nanoplatform for simultaneous photoacoustic imaging and photodynamic therapy.

A kind of inorganic prodrug, tellurium nanowires with enhanced ROS generation and GSH depletion, was developed for selective cancer therapy with high efficacy.

Water-soluble alloyed CdHgTe nanorods were synthesized in aqueous media using CdTe nanorods as a template. Their emission spectra were in the near-infrared and tunable according to material compositions (red-shifted with increased Hg content).

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LncRNA colon-cancer-associated transcript-1 (CCAT1) was proved to be a potential prognostic biomarker for breast cancer progression. However, the role of CCAT1 in regulating radiosensitivity of breast cancer and its underlying mechanism have not been investigated. The present study showed that CCAT1 was up-regulated and miR-148b was down-regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues. Radiation treatment triggered a significant increase in CCAT1 and an obvious decrease in miR-148b. CCAT1 down-regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation. Moreover, CCAT1 could negatively regulate miR-148b expression. Furthermore, overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. Taken together, this study demonstrated that CCAT1 down-regulation improved radiosensitivity of breast cancer cells via negatively regulating miR-148b expression, providing a crucial clue for lncRNA-miRNA interaction in the mechanism of radiosensitivity of breast cancer.