Chloride intracellular channel 1 regulates migration and invasion in gastric cancer by triggering the ROS-mediated p38 MAPK signaling pathway.

Mol Med Rep 12:[Related article:] 8041–8047, 2015; DOI: 10.3892/mmr.2015.4459 Following the publication of this article, an interested reader drew to our attention anomalies associated with the presentation of Fig. 4A. In the original presentation of the Figure, different representations of the same photomicrograph were inadvertently used for the panels labelled 'N', 'H-R', 'H-R + NAC' and 'H-R + SB203580'. This error arose as a consequence of an incorrect ordering of our original image numbers. A corrected version of Fig. 4A is provided below, featuring the appropriate data for each of the five panels listed above. This Figure was intended to show how, compared with the normoxic control group, the invasiveness of the SGC-7901 gastric cancer cells was markedly increased under hypoxia-reoxygenation (H-R) conditions, although pretreatment with N-acetyl cysteine (NAC; 30 mmol/l) or indanyloxyacetic acid 94 (IAA-94; 40 μmol/l), inhibited the invasiveness resulting from H-R exposure. Similarly, treatment with the inhibitor of p38 mitogen-activated protein kinase, SB203580 (10 μmol/l), also inhibited the cell invasiveness induced under the H-R conditions. We sincerely apologize for this mistake, and thank the reader of our article who drew this matter to our attention. Furthermore, we regret any inconvenience this mistake has caused.

Mol Med Rep 12:8041–8047, 2015; DOI: 10.3892/mmr.2015.4459

Following the publication of this article, an interested reader drew to our attention anomalies associated with the presentation of Fig. 4A. In the original presentation of the Figure, different representations of the same photomicrograph were inadvertently used for the panels labelled 'N', 'H-R', 'H-R + NAC' and 'H-R + SB203580'. This error arose as a consequence of an incorrect ordering of our original image numbers. A corrected version of Fig. 4A is provided below, featuring the appropriate data for each of the five panels listed above. This Figure was intended to show how, compared with the normoxic control group, the invasiveness of the SGC-7901 gastric cancer cells was markedly increased under hypoxia-reoxygenation (H-R) conditions, although pretreatment with N-acetyl cysteine (NAC; 30 mmol/l) or indanyloxyacetic acid 94 (IAA-94; 40 μmol/l), inhibited the invasiveness resulting from H-R exposure. Similarly, treatment with the inhibitor of p38 mitogen-activated protein kinase, SB203580 (10 μmol/l), also inhibited the cell invasiveness induced under the H-R conditions. We sincerely apologize for this mistake, and thank the reader of our article who drew this matter to our attention. Furthermore, we regret any inconvenience this mistake has caused.

Figure 4

CLICl is involved in the regulation of SGC-7901 gastric cancer cell invasion. Cells were treated with NAC (30 mmol/l), IAA-94 (40 μmol/l) or SB203580 (10 μmol/l) for 1 h and then exposed to H-R or normoxic conditions for 24 h. A Matrigel invasion assay was performed to examine SGC-7901 gastric cancer cell invasiveness. (A) Invaded cells were fixed and stained with crystal violet and observed under a microscope (magnification, x100). (B) Numbers of invaded cells were quantified under a microscope in five randomly-selected fields. Data are expressed as the relative number of invading cells compared with those under normoxic conditions and are presented as the mean ± standard deviation. **P<0.01, vs. normoxic group; ##P<0.01, vs. H-R group. N, normoxia; H-R, H-R, hypoxia-reoxygenation; IAA-94, indanyloxyacetic acid 94; NAC, N-acetyl cysteine.